rimed mesenchymal stem cells (MSCs) with lipopolysaccharide (LPS) on poly-l-lactic-acid nanoscaffold significantly enhanced MSCs proliferation and osteogenesis. Also the combination of LPS and electrospun nanofibers can provide a new and suitable matrix to support stem cells differentiation for bone tissue engineering.

Proinflammatory macrophages inhibited the expression of matrix anabolic genes, but increased the expression of inflammation-related genes as well as matrix catabolic genes, in rat nucleus pulposus (rNP) cells. Proinflammatory macrophages promoted the degenerative phenotypes in rNP cells in part through activating ERK and JNK signaling. Targeting ERK and JNK pathways may serve as a potential therapeutic approach for the treatment of intervertebral disc (IVD) degeneration.

Members of the B-cell translocation gene (BTG) protein family are important regulators of cellular differentiation and maintenance of homeostasis under conditions of cellular stress. This review describes these and other cellular functions, and highlights their emerging roles as potential tumor suppressors.

The morbidity of acute pericarditis is increasing overtime. Apart the known impairment of the adaptive immunity, recently a large body evidence indicated the central role of the innate immune system in the pathogenesis of recurrent pericarditis, starting from similarities with autoinflammatory diseases, with the “inflammasome” playing an important role. The role of the adaptive immune system in pericarditis cannot be reduced to a black or white issue as these mechanisms often overlap and new therapeutic strategies should be investigated in this direction.

MicroRNAs (miRNAs) regulate several biological and physiological processes in mammalian cells, including cellular proliferation, differentiation, apoptosis, and metabolism. Recent studies have confirmed the alteration of them during the cancer development. Matrix metalloproteinases (MMPs), belonging to the large family of proteases, have also been demonstrated to play crucial roles in tissue remodeling, and to support cancer progression and metastasis. There are several known miRNAs which regulate the MMP family and their expression. The expression profiles of miRNAs involved in MMP regulation, change during cancer progression and metastasis.

Novel optoelectronic instrumentation has been developed for the multispectral imaging of autofluorescence emitted by metabolic fluorophores. The images resolve individual cells while spectra are collected for each pixel in the images. To date, the system has been applied to fresh, ex vivo, human surgical specimens and has distinguished breast cancer (A) from benign tissue (B).

The development of innovative in vitro models is a growing need in the field of orthopedics and regenerative medicine. The present review aimed at critically revising the existing literature on osteochondral tissue culture models to identify a reference experimental set-up, applicable to the study of osteochondral lesions.

Inflammasome mechanisms are involved as some of the pathways of sterile inflammation. Nanoparticle-associated molecular patterns (NAMPs), which are mediated by synthetic materials, including nanomaterials and nanoparticles, are proposed to be new danger signals of NLRP3 inflammasomes. NLRP3: nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing 3

This review summarizes, miRNAs biology, functions, role of miRNAs in epigenetics and intercellular communication; Alteration of miRNAs after exercise, their association with diseases, and their therapeutic potential; Bioinformatics tools for miRNA studies and their analysis methods.

This review summarizes the current knowledge of the neural regulation of bone metabolism and homeostasis, as well as its role in skeletal diseases and discusses the emerging challenges presented in this field.

P68 or DDX5 is an RNA helicase that is dysregulated in breast cancer and can modulate the expression of several oncogenic factors in breast cancer. Therefore, it may be considered a potent therapeutic target in breast cancer.

The signal pathways in Sirt3-mediated autophagy when myocaridal ischemia–reperfusion (I/R) happened. We tend to find the novel relationship between Sirt3 and autophagy when myocardial I/R happened.

miR-15a/16 is an important tumor suppressor gene cluster in human cancers. miR-15a/16 takes part in a wide array of biological processes including tumor cell proliferation, apoptosis, invasion, and chemoresistance by binding to the 3′-untranslated region of its target gene's messenger RNA.

The p53 mutation favors Warburg phenotype by upregulating glycolytic proteins and flux and downregulating OxPhos proteins and flux under normoxia and may represent a gain-of-function mutation for glycolysis and a loss-of-function mutation for OxPhos.

Curcumin is a phytochemical with diverse biological properties that could contribute to accelerated wound healing. Formulation of curcumin into nanofibers created using electrospinning process has been suggested as a promising strategy to improve the delivery of curcumin to wound tissue. Here, we review the extant evidence on the use of synthesized curcumin nanofibers for the purpose of wound healing.

SII might serve as a noninvasive and powerful tool for predicting survival outcome in patients with GI cancers.

This review focuses on the latest research regarding the roles and mechanisms of the DIRAS family members in regulating Ras function, cancer development, assessing potential challenges, and providing insights into the possibility of targeting them for therapeutic use. Ingenuity signaling pathway analysis of cellular physiology (cell proliferation, migration, apoptosis, autophagy) by induction of DIRAS family members. DIRAS family members mainly regulate the PI-3K/AKT/mTOR, RAS/RAF/MEK/ERK, NF-κB, and JAK/STAT signaling pathways to inhibit cell proliferation and migration (light green ellipse) and induce apoptosis and autophagy (dark green ellipse). (Orange round represent DIRAS family members, pink round represent molecular upregulated by DIRAS family members, purple hexagon represent molecular downregulated by DIRAS family members, small yellow round represent molecular by phosphorylation, blue oval represent transmembrane receptor, and green square represent extracellular factor).

Rheumatoid arthritis (RA) is an autoimmune disorder with a number of risk factors, including both genetic and environmental, and a number of RA risk associated genomic loci has been identified. In this review, we summarize the association of genetic factors with RA reported in population studies in Iran; no significant association was found between the majority of genetic factors identified in other populations and risk for RA in the Iranian subjects. This conflicting result could be due to the ethnic differences and diversity that are present in Iran and we conclude that there is a need to investigate larger groups of Iranian subjects, encompassing different regions of Iran, to either prove or refute these initial findings.

Increasing evidence has implicated circular RNA (circRNA) in the pathogenesis of multiple cardiovascular diseases.This review provides scientists and clinicians with a brief summary of the ever-growing world of circRNAs and their role in cardiac diseases specifically.

The interactions and mutational profile of metabolic oncoregulators with energy metabolism in mutated Kirsten rat sarcoma viral oncogene homolog (KRAS) colorectal cancer.

Selective inhibitors or agents against metabolic targets or KRAS signaling may be clinically useful for consensus molecular subtype 3 tumor treatment through a cancer-patient-personalized approach.

In this review, we describe the anticarcinogenic effects of melatonin and also its possible application in clinical oncology.

Third-generation antibody–drug conjugates are more effective, showing lower levels of unconjugated monoclonal antibodies, more-stable linkers, improved pharmacokinetic properties, and safety profiles.

Autophagy is a self-degradative process that plays a pivotal role in several medical conditions associated with infection, cancer, neurodegeneration, aging, and metabolic disorders. Curcumin, as a hydrophobic polyphenol compound extracted from the known spice turmeric, is capable of triggering autophagy in several cancer cells.

This study mainly focuses on outlining different pathways involved in angiogenesis to clarify how these pathways and their connections may result in neutralization of antiangiogenic therapy with bevacizumab.

microRNAs have a very crucial role in tumorgenesis and prevention of cancer, which play a significant role in influencing various factors through different signaling pathways. microRNAs can act as tumor suppressors and oncomirs in this cancer through phosphoinositide 3-kinase/AKT signaling pathway.

Cyclooxygenase-2 (COX-2) is frequently expressed in many types of cancers exerting a pleiotropic and multifaceted role in genesis or promotion of carcinogenesis and cancer cell resistance to chemo- and radiotherapy. COX-2 is released by cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and cancer cells to the tumor microenvironment (TME). COX-2 induces cancer stem cell (CSC)-like activity and promotes apoptotic resistance, proliferation, angiogenesis, inflammation, invasion, and metastasis of cancer cells.

Cross-talks between various cells in the stroma of tumor microenvironment (TME) in favor of or against of tumor progression. Release of a variety of proteins, transcription factors, cytokines, chemokines, and so forth from cells inside the TME direct the fate of cancer. Concentration of these TME components along with temperature, circadian rhythm, and pH inside this microenvironment determine the fate of signaling. Complexity of the TME is a reason for failure of most of the conventional therapies against cancer.

This review illustrates the role of propranolol in fear memory with demonstration of studies that support or oppose its beneficial effect.

The half-life of transplanted kidneys is <10 years. Acute or chronic rejections have a negative impact on the transplant outcome. Therefore, achieving to allograft tolerance for improving long-term transplant outcome is a desirable goal of the transplantation field. The main reason for allograft loss is the immunological responses. In the present study, we are going to review and discuss the immunological characteristics of renal transplant recipients with rejection and compare them with tolerant subjects.

In nature, MT participates in many physiological and pathological processes including embryonic development, organogenesis, wound healing, and cancer metastasis. Many aspects regulate EMT including: transcription factors, gene expression patterns, and signaling pathway crosstalk. MicroRNAs as noncoding genes play a distinct role in the progression or suppression of EMT.

In this narrative review, the pathophysiology of albuminuria in patients with diabetic nephropathy is discussed. Furthermore, the renoprotective effects of antidiabetic drugs, focusing on albuminuria, are reviewed.

• Additional chromosomal aberrations may cause different features on chronic myeloid leukemia (CML) patients according to Philadelphia translocation pattern.

• Karyotype analysis in CML patients with complex karyotype shows unrandom pattern.

• Incidence of additional chromosome and variant translocation is higher in blast crisis of CML.

The Mediterranean diet (MedDiet) exerts a protective effect on the different components of metabolic syndrome. Interestingly, the polyphenols contained within the representative components of MedDiet seems to be responsible for the beneficial properties associated to this dietary pattern.

Intervention of Eucalyptol protects lungs against bacterial invasion of tobacco smoke-exposed lungs. The protection role of Eucalyptol in the tobacco smoke-exposed lungs was realized by attenuating ciliated cell damage and suppressing MUC5AC protein and gene expression.

In the present study we define and compare the molecular mechanisms linking adenosine- and ATPγ-induced purinergic receptor activation and barrier strengthening in HLMVECs. We found that ATPγS-induced EC barrier enhancement is EPAC1-independent and is instead mediated by activation of PKA which is then guided by AKAP2, in a cAMP-independent mechanism, to activate MLCP and dephosphorylate MLC20 resulting in reduced EC contraction.

The increased life expectancy of HIV-1 infected people is accompanied by a higher prevalence of HIV-1 associated neurocognitive disorders. HIV-1 infection increases extracellular deposits of amyloid beta protein in primary cutures of human astrocytes. The presence of HIV-1 in the brain could contribute to the increase of the total burden of cerebral Aβ.

The possible interactions between different signaling pathways in glioblastoma cells treated with Pt3glc, which inhibited glioblastoma cell proliferation and promote apoptosis by regulating the expression of SIRT3 and down-regulating the p53 through ROS/p53-mediated mitochondrial pathway via SIRT3. The combination of Pt3glc with LY294002 could produce the synergistic effect to inhibit the SIRT3-mediated glycolytic as well as regulation of mTOR/Akt pathway. Pt3glc appears to play a central role in regulating SIRT3 for glioblastoma cell death, thus qualifies as a potential target for anti-cancer treatment.

This study aims to investigate the effect of polo-like kinase 1 (PLK1) inhibition on cisplatin (DDP)-resistant gastric cancer (GC) cells. Together, our experimental results illustrated that the DDP resistance of GC cells might be associated with the aberrant overexpression of PLK1. PLK1 inhibition, including si-PLK1 and BI2536 treatment, could restore the chemosensitivity of drug-resistant SGC-7901/DDP cells and enhance the efficacy of DDP, revealing the potential value of PLK1 inhibition in GC chemotherapy.

MicroRNA-21 inhibits Sprouty-1 to promote the progression of fibrosis in peritoneal mesothelial cells by activating the rennin angiotensin system–mitogen-activated protein kinase signaling pathway.

Purple sweet potato color (PSPC) delays endothelial senescence by promoting autophagy. Autophagy receptor colocalizes with nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome. Autophagosomes induced by PSPC target the NLRP3 inflammasome and deliver it to the lysosome for degradation.

This was the first time that we clearly simulated the Notch1 activities by blocking its processing and determined the ability of unprocessed Notch1 to signal. These data emphasized the significant role of epidermal growth factor receptor–phosphoinositide 3-kinase–protein kinase B signaling in Notch1-mediated oncogenesis and could explain the potential mechanism underlying membrane-tethered Notch1-related phenotypic alterations.

Tumor necrosis factor-α–tumor necrosis factor receptor signal pathway was involved in the occurrence and development of coal worker's pneumoconiosis by activating FAS–caspase-8 and thus inhibiting autophagy while promoting apoptosis of AM.

Overexpression yes-associated protein 1 (YAP1) decreased Sox-9, Col-II, aggrecan expression, whereas increased matrix metalloproteinases 13 level in NP cells. Interleukin 6 (IL-6) enhanced YAP1 and β-catenin interaction and nuclear accumulation, β-catenin was essential for IL-6/YAP1 signaling induced intervertebral disc degeneration (IDD). Moreover, we found that verteporfin, an FDA approved drug, effectively alleviated IDD development.

We aimed to explore the impact of long noncoding RNA (LncRNA) nuclear enriched abundant transcript 1 (NEAT1) on cell proliferation, invasion, and migration of glioma. The results of our study showed that LncRNA NEAT1 promotes cell proliferation, invasion, and migration of glioma through regulating miR-139-5p/CDK6 pathway.

Perindopril may have better short-term effects on reducing blood pressure and expression of inflammatory factor, while quinapril may have better long-term effects on reducing blood pressure and expression of inflammatory factor.

We defined the promoter region of human interleukin-21 (IL-21) gene and identified different mechanisms, including Sp1 and NFATc2 transcription factors. Acetylation status of histones and miR-302c is be involved in regulating the IL-21 expression. These molecular mechanisms could, therefore, be targeted to manipulate IL-21 expression in the context of disease treatment.

Spinal cord injury (SCI) is one kind of severe traumatic injury, resulting in systemic inflammatory response syndrome and secondary lung injury, which is an important pathological basis of respiratory complications. Our data reveal that nucleotide-binding domain-like receptor protein 3 inflammasome inhibitor BAY 11-7082 or A438079 attenuates the inflammatory response, reverses mitochondrial dysfunction, and subsequently alleviates secondary lung injury following SCI.

Downregulated microRNA-27b (miR-27b) could promote NF-E2-related factor 2 (Nrf2), which exerts a protective effect on acute lung injury caused by lipopolysaccharide (LPS) via inhibiting the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway.

This study demonstrates that downregulation of miR-592 prevents CHD and hypoplastic heart by inhibition of the Notch signaling pathway via negatively binding to KCTD10.

Our findings reveal a novel mechanism by which miR-186 inhibits chondrocyte apoptosis in osteoarthritis (OA) by interacting with SPP1 and regulating PI3K–AKT pathway. Restoring miR-186 might be a future therapeutic strategy for OA

The ketotic cows displayed hepatic lipid metabolic disorder and high blood concentration of glucagon. The present study indicates that glucagon activates the AMPK signalling pathway to increase lipid oxidation and VLDL assembly and decrease lipid synthesis in cow hepatocytes, thereby reducing liver fat accumulation.

In this study, we have shown for the first time that histone deacetylase 8 (HDAC8) is expressed in human and zebrafish skeletal muscles specifically in an advanced stage of muscle differentiation. The HDAC8 inhibition through a specific PCI-34051 inhibitor in murine C2C12 myoblasts and zebrafish embryos led to skeletal muscle differentiation impairment. We also found a positive regulation of the canonical Wnt signaling by HDAC8 that might explain muscle differentiation defects.

Prolactin (PRL) binding with PRL receptor stimulates the activation of JNK, which facilitates the formation of the complex of JNK-Tudor staphylococcal nuclease (Tudor-SN). JNK further activates the phosphorylation of Tudor-SN, which promotes the nuclear transport of Tudor-SN. Then, activated Tudor-SN positively regulates the proliferation of bovine mammary epithelial cells and milk production.

SPARC was mainly expressed in the villous and extravillous cytotrophoblastic cells in first trimester, whereas in PE, PE–IUGR and at term placentas, SPARC immunostaining was visible in both cytotrophoblastic cells and syncytiotrophoblast. SPARC expression significantly decreased in normal placenta from first to third trimester and a further significant reduction was demonstrated in PE and PE–IUGR. The latter downregulation of SPARC depends on hypoxic condition as shown by in vitro models.

In this study, we used a nanosystem based on poly (D, l-lactide)–polyethylene glycol (PLA–PEG), for the delivery of galbanic acid (GBA) to C26 colon carcinoma cells. The results suggest that the encapsulation of GBA into the PLA–PEG could potentially be used for the treatment of colorectal cancer

In vivo confocal microscopy (IVCM) and anterior segment optical coherence tomography (AS-OCT) are diagnostic devices useful to analyze neurotrophic keratopathy (NK). Based on the IVCM and AS-OCT results, a new classification of NK can be proposed. According to this classification, important information about prognosis, follow-up, and therapeutic approach can be achieved

In our study, we found that silencing of LINC01433 repressed hepatocellular carcinoma (HCC) progression by sponging miR-1301. In addition, STAT3 could act as a direct target of miR-1301, and miR-1301 mimics inhibited STAT3 expression significantly in HCC cells. Our data suggested that the LINC01433/miR-1301/STAT3 axis was involved in HCC progression and LINC01433 might serve as a biomarker for HCC.

Active autophagy was observed in perinatal ovaries from 16.5 dpc to 3 dpp, and the physiological level of autophagy in perinatal ovaries regulates germ cell cyst breakdown and primordial follicle assembly by ROS clearance and exerts extensive effects on further follicular development.

Our study demonstrates that stromal vascular fraction cells combined with dual sustained release VEGF/ANG-1-PLGA microspheres can improve angiogenesis and graft survival. Nude mice treated with stromal vascular fraction cells and the microspheres developed in this study exhibited reduced fibrosis and increased microvascular density. These findings provide a practical method for improving graft survival after autologous fat transplantation.

In the current study, we show that subtoxic concentrations of selected snake venoms promote FOXO3a-mediated oxidative stress response and to a lesser extent DNA damage response that results in changes in the levels of cell cycle regulators leading to cell cycle arrest and stress-induced premature senescence (SIPS) in human fibroblasts in vitro.

• 1.

  This study illustrates the molecular interaction between nuclear paraspeckle assembly transcript 1 (NEAT1), miR-23a, and structural maintenance of chromosome 1 alpha (SMC1A) in acute myeloid leukemia (AML).

• 2.

  Reduced expression of NEAT1 induced the tumorigenesis and progression of AML through the miR-23a-3p/SMC1A axis.

• 3.

  These results suggest that this axis can be used as a promising therapeutic target to mitigate the progression of AML.

The findings indicate microRNA (miR)-874 as a contributory role in cardiac ischemia–reperfusion injury (I/R) injury, with miR-874 inhibition alleviating cardiac I/R injury in mice following sevoflurane pretreatment by targeting signal transducer and activator of transcription 3 (STAT3) through the Janus kinase 2 (JAK2)/STAT3 signaling pathway.

H₂O ₂ alters MuRF1/LC3b/cathepsin/calpain/caspase-3-dependent proteolytic systems. Cinnamaldehyde (CNA) ameliorates the altered proteolytic systems. CNA normalizes the antioxidant enzymes level in H ₂O ₂-treated cells. CNA shows its protective effect against H ₂O ₂-induced myotube atrophy by suppressing multiple dysregulated pathways

Tie2 C-terminal tyrosine 1106 is indispensable for the maintenance of the stemness features of bone marrow endothelial progenitor cells (EPCs). Missense mutation in the codon encoding tyrosine 1106 of Tie2 prompts a phenotypic switching in bone marrow EPCs. Tie2 C-terminal tyrosine 1106 restores the potency of bone marrow–derived EPCs for bone marrow reconstitution after myelosuppression.

The benzo[ghi]perylene can reduce the quality of oocytes by disrupting cytoskeletal integrality, chromosome euploidy, and mitochondrial functions, whereas melatonin has a certain protective effect on preventing the reduced oocyte quality during meiotic maturation.

In this study, the methylation status of the promoter region of ZBTB16 and Twist1 genes and their role in controlling osteoblastic differentiation in mesenchymal stem cells (MSCs) were investigated during the osteoblastic differentiation of MSCs.

Mll2- and Mll3-COMPASS complexes bind to the Runx2-P1 promoter region in osteoblastic cells to control the transcription of this master regulator of osteogenesis.

We found that DiGeorge syndrome critical region gene 5 (DGCR5) expression was significantly downregulated in bladder cancer (BCa) tissues compared with adjacent normal tissues. Our study demonstrated that DGCR5 transcriptionally promotes P21 expression to suppress BCa progression.

Exogenous transforming growth factor-β (TGF-β1) is added into neonatal mouse cardiac fibroblasts, triggering promyelocytic leukemia (PML) SUMOylation and PML nuclear bodies (NBs) formation. Meanwhile, Pin1 is recruited into the PML-NBs and colocated in the nuclear body. Then, the messenger RNA level and protein level of TGF-β1 are both increased, activating the TGF-β/Smad-2/3 signaling pathway, increasing collagen formation, and ultimately leading to cardiac fibrosis.

The current study demonstrates that lysophosphatidic acid (LPA) promotes the interaction between the endovascular human first trimester trophoblast and endothelial cells at the maternal–fetal interface. This crosstalk depends on the secretion of LPA-induced trophoblast soluble factors belonging to cyclooxygenase-2 and IL-6 pathways. Our findings shed new light on the significance of LPA signaling in the vascular events that lead to a successful pregnancy.

In this paper, we revealed a mechanism that ten-eleven translocation 1 (TET1) regulated hypoxia-inducible factor-1-alpha (HIF-1α) and targeted hypoxia-responsive genes through interfering the binding of HIF-1α to their hypoxia-responsive elements by enhancing promoter methylation. We also identified two novel TET1 gene mutations in 120 paired tumor/normal tissue specimens and found that TET1 E2082K mutant blocked the TET1-enhanced migration. Because hypoxia prevails on solid tumors, by demonstrating the mechanism that TET1 regulated HIF-1α-responsive genes, we showed that epigenetic mechanism and tumor microenvironment-driven models coexisted and mutually affected.

Endometriosis is a chronic gynecological inflammatory disorder in which immune system dysregulation is thought to play a role in its initiation and progression. In the current study, we examined the effects of curcumin (CUR, diferuloylmethane ), an anti-inflammatory folk medicine in Asian countries, on eutopic endometrial stromal cells derived from woman with or without endometriosis. The basal level of proinflammatory and proangiogenic chemokines and cytokines expression were higher in primary cultures of stromal cells derived from eutopic endometrium of endometriosis (EESC) subjects compared with normal endometrial stromal cells (NESC). The treatment of EESC and NESC with CUR significantly and dose-dependently reduced chemokine and cytokine secretion over the time course. Notably, CUR treatment significantly decreased phosphorylation of the IKKα/β, NF-κB, STAT3, and JNK signaling pathways under these experimental conditions. Taken together, our findings suggest that CUR has therapeutic potential to reduce inflammation associated with endometriosis.

Evidence suggests that overfeeding after nutrient deprivation may favor the disruption of metabolism and, therefore, favor the development of obesity, type 2 diabetes, and comorbidities. In animal models, the effects of fat-enriched diets in protein-restricted mice are still controversial. Protein restriction programmed skeletal muscle metabolism increased mitochondrial function and prevented fat accumulation and increment on fasting plasma glucose and insulin concentration.

The role of 2-methoxyestradiol (2-ME) was investigated in a model of pulmonary hypertension (PH) induced by chronic intermittent hypoxia. We found that 2-ME markedly reduced PH progression, and this effect is associated with reduced microRNA-223 (miR-223).

The results of this study indicated that EB30 could decrease cell viability, induce apoptosis, and cell cycle arrest. The induction of apoptosis was found to be mediated through the mitochondrial intrinsic pathway and extrinsic pathway. The apoptotic effects of EB30 were mediated by suppressing the PI3K/Akt pathway, whereas activating the ERK1/2 signaling.

Gastric cancer (GC) is one of the most fatal cancers in the world. Thousands of biomarkers have been explored that might be related to survival and prognosis via database mining. We aimed to develop a novel gene signature to improve the prognosis prediction of GC. In conclusion, we developed a five-gene signature related to the cell cycle that can predict survival for GC.

Pyruvate dehydrogenase kinase 1 (PDK1) was upregulated in cisplatin-resistant ovarian cancer. PDK1 knockdown in resistant ovarian cancer cells led to increased sensitivity to cisplatin-induced cell death and apoptosis, and reversed the epithelial–mesenchymal transition (EMT) and cell motility. There was a feed-forward PDK1/EGFR crosstalk in ovarian cancer cells that drives cisplatin resistance in terms of both cellular growth and EMT.

Curcumin regulates cellular redox status depending on cell sensitivity and/or curcumin concentration in normal cells. Mitochondria respond differentially depending on curcumin concentration-dependent induction of ROS. Curcumin may be an effective therapeutic target for diabetes and other mitochondrial diseases when used in low concentrations.

Epigenetic-reprogramming of TIMP1 emerges as critical element in smooth muscle cells mechanotransduction and as epigenetic machinery is amendable to pharmacological manipulation, this pathway may have important clinical consequences.

The mitochondrial cytochrome oxidase (CO) genes are involved in complex IV of the electron transport system (ETS), and dysfunction of CO genes leads to several diseases. nHowever, no work has been reported on the codon usage pattern of these genes. We used bioinformatic methods to analyze the compositional properties and the codon usage pattern of the COI, COII, and COIII genes in fishes, birds, and mammals to understand the similarities and dissimilarities of codon usage in these genes, which gave an insight into the molecular biology of these genes.

Endoplasmic reticulum stress caused by Iturin A-like lipopeptides human epithelial colorectal adenocarcinoma (Caco-2) cells the appeared reaction, resulting in the increase of intracellular calcium and swelling and dysfunction of mitochondria. A large number of vacuoles appeared in the cell, and the parabed apoptosis occurred. Reactive oxygen species (ROS) was released in mitochondria, DNA was damaged and mitochondria permeability increased. Then the endogenous apoptosis pathway is triggered. A large number of damaged organelles and proteins in the cell lead to the activation of autophagy pathway.

c-Src phosphorylates HDAC3: Phosphorylation of HDAC3 by c-Src regulates cancer cell proliferation

This study describes the designing of a chimeric vaccine which was developed by assembling helper T lymphocytes, cytotoxic T lymphocytes, and B-cell epitopes. Our observation suggests the immunogenic nature of the designed vaccine candidate.

Using weighted gene coexpression analysis, YWHAB was identified and validated in association with IPAH progression, which might serve as a biomarker and/or therapeutic target for IPAH.

Acute lung injury and its severe form acute respiratory distress syndrome remain a major cause of morbidity and mortality in critically ill patients, and no specific therapies are still available to control the mortality rate. In this study, our results demonstrated that tannic acid, a natural polyphenol treatment attenuated lipopolysaccharide-induced inflammatory response and oxidative stress by blocking toll-like receptor 4 expression and mitogen-activated protein kinase activation

Helvolic acid (HA), a mycotoxin originally isolated from Aspergillus fumigatus, is demonstrated to be capable of significantly inhibiting receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and bone resorption in vitro by suppressing nuclear factor of activated T cells 1 (NFATc1) activation without affecting nuclear factor-κB (NF-κB) activation. Mechanistically, HA greatly attenuated multiple upstream pathways of NFATc1, including extracellular-signal-regulated kinase (ERK) phosphorylation, c-Fos signaling, and intracellular Ca²⁺oscillation. Taken together, HA can be potentially used in the development of a novel drug for osteoclast-related bone diseases.

The overall gene expression in human embryo drastically changes from the eight-cell stage onward. Dynamic changes observed in the transcription factors (TFs) expression at the first division of the embryo. More than 200 TFs were involved in the transition from the eight-cell stage.

Hypoxia induces hypoxia-inducible factor-1α (HIF1α) and zinc finger E-box binding homeobox 2 (ZEB2) in podocytes. HIF1α induces the expression of ZEB2 in podocytes. ZEB2 overexpression ensures podocyte foot-processes effacement and proteinuria.

In this study, we performed whole-genome methylation analysis of LUSC patients based on the TCGA database. Univariate and multivariate Cox regression analysis showed that the prognostic risk model constructed by four abnormally methylated genes (VAX1, CH25H, ADCYAP1, and IRX1) proved to be an independent prognostic factor for LUSC. Also, the expression and methylation levels of the key gene IRX1 are significantly correlated with prognosis and are negatively correlated with the methylation of the site cg09232937 and cg10530883. This study is based on high-throughput data mining and provides an effective bioinformatics basis for further understanding the pathogenesis and prognosis of LUSC, which has important theoretical significance for follow-up studies on LUSC.

Inhibiting c-Jun N-terminal kinase (JNK1)/2 activation significantly inhibited ubiquitin-specific peptidase 49 (USP49) knockdown-induced the cell viability inhibition, apoptosis, and the JNK1/2 activation in AC16 cardiomyocytes. USP49 positively regulated dual-specificity protein phosphatases 1 (DUSP1) expression through deubiquitinating DUSP1. USP49 as a novel regulator of DUSP1–JNK1/2 signaling pathway with a protective role in cardiac I/R injury.

New peptide Scp01-b with more residues compared to conventional cell-penetrating peptides (CPPs), and this cell-permeable peptide can efficiently mediate nucleic acid intracellular delivery, acting as a powerful DNA carrier for non-viral-based reprogramming in regenerative medicine and the field of gene editing research

Long noncodingRNA colorectal neoplasia differentially expressed (CRNDE) could facilitate hepatocellular cancer (HCC) cell propagation, invasiveness, and migration through regulating miR-203/ BCAT1 axis. This finding not only disclosed the regulatory mechanism of CRNDE/miR-203/BCAT1 network in HCC, but also provided novel biomarkers and therapeutic targets for the clinical diagnosis and treatment of HCC.

Our data provided a comprehensive report on the profile and dynamic changes of the liver proteins in AILI; the involvement of Gzmf and the role of Stat3 in necrosis were revealed; and the role of hepatocyte in liver self-repair was well clarified.

The ‘neonatal’ splice variant of Nav1.5 is shown to drive the invasiveness of human colorectal cancer cells under normoxic and hypoxic conditions. Ranolazine, an inhibitor of the persistent current of the channel, inhibits the hypoxia-induced increase in invasiveness.

We found that highly expressed X-inactive specific transcript (XIST) is associated with poor overall survival in human cancers. Highly expressed XIST is associated with lymph node metastasis, tumor size, differentiation and clinical stage, but not with age or gender. XIST might serve as a potential novel biomarker for predicting the clinical outcomes in human cancers.

In the current study, microRNA-382-5p was identified as a regulator of mitochondrial biogenesis and dynamics at mRNA levels. Silencing of miRNA-382-5p in C2C12 myotubes revealed a collective downregulation of mitochondrial ribosomal proteins and respiratory chain proteins. MiR-382 silenced C2C12 showed a mitonuclear protein imbalance that led to the activation of the mitochondrial unfolded protein response and a reduced basal oxygen consumption rate without affecting mitochondrial content.

Upregulated chloride channel-3 induced by chemotherapeutic drugs activates the nuclear factor-κB (NF-κB)-signaling pathway and leads to the nuclear translocation of NF-κB P65. This consequently enhances the transcriptional activity of multidrug resistance 1, ultimately increases P-glycoprotein expression, and promotes the efflux of chemotherapeutic drugs.

“Small nucleolar RNA host gene 12 (SNHG12) might be a novel biomarker for the diagnosis or treatment of cervical cancer and SNHG12/miR-125b/ signal transducer and activator of transcription 3 axis was implicated in the progression of cervical cancer.”

We found Gm6135 negatively regulated relative expression of miR-203, stimulated expression of toll-like receptor 4 (TLR4) and promoted cell proliferation of SV40-MES-13 cells. Our study proved that the Gm6135/miR-203/TLR4 axis played an important role in diabetic nephropathy (DN) and provided a novel perspective for the pathogenesis of DN.

Preventative intranasal administration of interleukin-27 (IL-27) can recruit more IL-27-secreted monocytes to the airway and change the different T-cell classes in lung. The improved type 1 T helper (Th1) environment helps to alleviate type 2 T helper (Th2)-mediated allergic asthma by repairing the signal transducer and activator of transcription 1 (STAT1) pathway but not the STAT4 pathway.

miR-335-5p enhanced insulin resistance and suppressed pancreatic islet β-cell secretion by inhibiting VASH1, eventually activating the TGF-β pathway in GDM mice, which provides more clinical insight on the GDM treatment.