miR-125b is an important microRNA in cancer. It is deregulated in different types of cancer where it acts as an oncogene and/or a tumour suppressor in a context-dependent manner. miR-125b interacts with multiple upstream regulators and downstream targets, which are involved in a variety of signalling pathways and cellular processes during tumourigenesis and cancer progression. It also exerts as a key regulator with regards to the response of cancer cells to chemotherapy. miR-125b holds a great potential in clinical cancer diagnosis, prognosis and therapies. Created with BioRender.com.

Growing evidence suggests that there is a correlation between the activation of nuclear factor (NF)-κB and the angiogenesis of glioma. Herein, we sought to discuss the current understanding of the molecular mechanisms of NF-κB in diverse glioma microenvironments such as hypoxia, inflammation, and oxidative stress, and its function as a therapeutic target for antiangiogenic strategies aimed at glioma.

Epigenetic therapeutics targeting cancer stem cells.

In current review, we accumulated literature to the understanding of lncRNAs biogenesis and function, as well as the latest findings of novel lncRNAs-based therapeutics in TNBC. We also present the current state of knowledge concerning the expression and regulation of lncRNAs in TNBC, and discuss the future development of lncRNA-based strategies for clinical TNBC patients.

As a regulatory element on the genome, the formation of super enhancers depends on specific chromatin states and spatial structures. A large number of regulatory molecules gather in the chromatin regions where the super enhancers are located. The molecules in these regions are very dense, forming huge transcriptional activation complexes, which interact with each other to construct phase-separated condensates. Super enhancer-mediated transcriptional activation depends on spatial proximity rather than a rigid bridge. There are molecular exchanges between the super enhancer-associated condensate and the surroundings. Inactive Pol II is recruited and phosphorylated Pol II is excreted. Therefore, we propose a super enhancer-mediated transcription mode to pave the way for future research.

Signal transducer and activator of transcription 3 (STAT3) is a member of the STAT protein family, vitally important for eukaryotic cells. We review the molecular structure and function of STAT3 and its isoforms, highlighting signalling pathways for the regulation of gene transcription. A critical appraisal of STAT3 in cancers, such as osteosarcoma, is provided emphasizing potential therapeutic approaches targeting STAT3 and its inhibitors

M2 macrophage infiltration and IL-33 production are enhanced with close correlation in ESCC. (A) Representative images of IL-33⁺ cell, CD206⁺ cell and CD68⁺ cell in non-tumour and tumour tissue (scale bar = 50 μm). (B) Western blot analysis of IL-33 and CD206 expression in non-tumour and tumour tissues, and GAPDH was used as a reference control. (C) IL-33, CD206 and CD68 were measured by RT-PCR in non-tumour and tumour tissues; the correlation of CD206 and IL-33 in ESCC tissues; N = 20, R² = .54, P < .01. (D) M1 (CD68⁺ CCR2⁺) and M2 (CD206⁺ CX3CR1⁺) populations in peripheral blood from those with ESCC (n = 48) and healthy controls (n = 33), as measured by flow cytometry. The difference in M1/M2 ratio between two groups was analyzed. (E) The population of M2-like monocytes subset in peripheral blood between ESCC patients and healthy controls showed significant difference instead of M1-like monocytes. (F) ROC curve was used to analyse to assess the diagnostic value in ESCC. *P < .05; **P < .01; ***P < .001. Bars indicate mean and SEM of triplicate experiments and show a representative experiment of at least 3 independent experiments performed for each panel.

MC-LR was able to inhibit the activity of PP2A and activate MEK-ERK signalling pathway via up-regulating the expression of SET, resulting in the ICC cell proliferation and poor prognosis.

Schematic representation shows the mechanisms of Kcnh2-modulated cardiac dysfunction following sepsis stimulus. Sepsis-induced decrease of Kcnh2 resulted in inhibition of AKT in cardiomyocytes. Attenuation of AKT of cardiomyocytes mediated by Kcnh2 upregulated FOXO3A expression, which initiated the transcription of BIM/PUMA genes. Finally, enhanced BIM/PUMA caused the cardiomyocytes apoptosis, leading to cardiac dysfunction.

The mechanism on 20-HETE–induced alterations of mitochondrial dynamics in neurons. 20-HETE is synthesized from AA by CYP4A, which is inhibited by HET0016. The alterations of mitochondrial dynamics induced by 20-HETE activate oxidative stress and subsequently result in neuronal apoptosis mediated by inhibition of the Sirt1/PGC-1α signalling pathway.

The epidermal growth factor receptor variant type III (EGFRvIII) mutation mostly found in high-grade astrocytoma in the brain, suggesting connection of EGFRvIII to astrogenesis. Using human brain organoids, we demonstrated that EGFRvIII mutation facilitated astrogenesis at the expense of neurogenesis and cell proliferation. In summary, this study shows for the first time the close connection between EGFRvIII mutation and gliogenesis in human system.

Single-cell RNA sequencing was used to characterize the transcriptomes of decidua before and after delivery. Eight major cell types and sixteen clusters were identified and found to have various functions. The activation of various cell subtypes to different degrees was observed after delivery. These reveal the heterogeneity of peripartum decidual cells at single-cell resolution

The schematic diagram shows the distinct pathogenesis between early- (EOPE) and late-onset pre-eclampsia (LOPE). The difference between EOPE and LOPE is demonstrated at several layers, such as risk factors, signalling pathways and disease affected/causing tissues. Based on divergence of EOPE and LOPE pathogenesis, specific biomarkers can be identified and used to distinguish both diseases by testing placental secreted proteins or maternal blood cell transcripts.

The graphical abstract demonstrated that short-term application of bFGF in the early stage post-thawing could rescue cellular viability without shifting their pluripotency, unexpectedly, this proliferative superiority could prolong to the succeeding passage, so the usage time of bFGF for post-thawed cell culture should be addressed. This study illustrated a safe and feasible cell culture technique to rapidly amplify post-thawed DPSCs with robust regenerative potency, which brightening the future of stem cells banking and tissue engineering.

Under HG conditions, FoxO1 acetylation level was increased. As a transcription factor, FoxO1 involved in the induction of a special subset of genes that regulate cellular proliferation or apoptosis, etc Increased Ski protein increased the binding of Ski to FoxO1, which mediated deacetylation through Ski binding with HDAC1 and resulted in a reduction in FoxO1 acetylation level. Therefore, the role of FoxO1 transcription factor was inhibited.

NLRP3 Regulates Alveolar Bone Loss in Ligature-induced Periodontitis by Promoting Osteoclastic Differentiation. Bacterial infection in periodontal tissues leads to the activation of NLRP3 inflammasome in osteoclast precursor cells, which promotes osteoclast differentiation and alveolar bone resorption. Thus, NLRP3 inflammasome contribute significantly to the pathologic bone loss in periodontitis. MCC950, a specific inhibitor of the NLRP3 inflammasome, inhibits osteoclast differentiation, thereby reduces alveolar bone loss in periodontitis.

With high-glucose treatment, the expression of HuR is decreased, which induces autophagy inactivation and increased senescence. Mechanistic study reveals that HuR regulates Atg7 expression through binding to Atg7 AU-rich element and adjusting its mRNA stability

In the endometrium of pregnant mammals, YAP activation promoted endometrial cell proliferation, induced EMT progression and supplied a weak inflammation benefit for uterus to receive the embryo. Mechanistically, expression levels of YAP were double regulated by upstream biochemical and mechanical signals in bEECs and partially dependent on the Hippo signalling pathway.

HepaRG cells serve as a useful model of hepatic differentiation. A novel lncRNA (lnc-RHL) is induced when bipotent hepatic progenitor cells are induced to differentiate. Using inducible knockdown approaches, we show that lnc-RHL regulates the final stage of liver development in which hepatocytes and cholangiocytes are formed from bipotent progenitor cells. Deficiency for lnc-RHL alters the balance of hepatocytes and cholangiocytes over the course of differentiation.

Compression stress induced the RhoA/ROCK1 pathway activation, which regulated the interaction of myosin IIA and IIB with actin. The actomyosin cytoskeleton remodelling was involved in the compression stress-induced fibrotic phenotype mediated by MRTF-A nuclear translocation and inhibition of proliferation in human NP cells.