BPIFB1 plays a pivotal role in promoting macrophage M2 polarization, which enhances the ability of hormone receptor-positive breast cancer cells to metastasize.

Talazoparib and palbociclib combination triggers therapy-induced senescence and activates antitumor immunity, which strengthens the anticancer effect of immune checkpoint blockade treatment in colorectal cancer. Characterization of senescence-associated secretory phenotype components reveals type I IFN-related mediators, which are amplified by cGAS/STING signaling.

Our results suggest that N-acetyltransferase 10 (NAT10) acts as an oncogene in oral squamous cell carcinoma (OSCC), and targeting N4-acetylcytidine (ac4C) acetylation could be a promising therapeutic strategy for OSCC treatment.

Development of novel tracers for sentinel node identification in uterine cancer. Indocyanine green (ICG)-phytate-liposome (LP) may be a useful new tracer for gynecological cancers that require time for lymph node identification due to a retroperitoneal approach.

We reveal the regulatory role and mechanism of B7H3 in inhibiting ferroptosis in colorectal cancer (CRC) cells. Depletion of B7H3 in CRC cells promotes ferroptosis through AKT/sterol regulatory element binding protein 2 pathway-mediated cholesterol metabolism.

ZNF500 is elevated in breast cancer, whose expression significantly negatively correlated with advanced TNM stage, positive lymph node metastasis and poor prognosis. ZNF500 binds to the C-terminal domain of P53 directly via its C2H2 domain, which may block the interaction between MDM2 and P53, thus stabilizing P53. Overexpression of ZNF500 accelerated DNA damage and sensitized chemotherapy treatment, which was confirmed in human breast cancer with neoadjuvant chemotherapy.

We found that Exos released by AIPC cells could acclimate ADPC cells to progressing to more aggressive cell types through the paracrine signaling system. Exos-miR-222-3p promoted ADPC cells transformed to AIPC-like cells, at least in part, by activating the mTOR signaling pathway by targeting MIDN. The current work underscores the great therapeutic potential of targeting Exo miRNAs, either as a single agent or in combination with the AR pathway inhibitors in the treatment of CRPC.

On the one hand, BCKDK can directly affect RCC metastasis by regulating the MEK-ERK signal. On the other hand, the new BCKDK/Exosomal miR-125a-5p/VE-cadherin signal axis provides a new understanding of RCC angiogenesis, markers, and potential therapeutic targets for anti-angiogenesis therapy of advanced RCC.

COL17A1 promoted or suppressed the tumorigenicity of KPC and AK4.4 cells, respectively, in vivo without affecting their proliferation in vitro. Tumor tissues exhibited distinct gene expression profiles including Wnt signaling and Hippo signaling between C57BL/6-KPC and FVB-AK4.4 models. COL17A1 promotes or suppresses cancer progression in a manner dependent on the interaction of tumor cells with the tumor microenvironment.

Our study reveals the essential role of YTHDF2 in gallbladder cancer (GBC). YTHDF2 was identified as the most significantly upregulated m6A-related gene in GBC and increases the mRNA degradation of the tumor suppressor DAPK3 in an m6A-dependent way, which promotes GBC progression and reduces its response to gemcitabine. These findings highlight an m6A-dependent molecular mechanism of GBC progression and provide new insights into the development of effective therapeutic approaches for GBC.

We screened the transcription factor basonuclin 1 (BNC1) to be highly expressed in esophageal squamous cell carcinoma (ESCC) by transcriptome sequencing of clinical samples and found that silencing BNC1 inhibited the malignant proliferation and metastasis ability of ESCC in vitro and in vivo. Furthermore, other experiments such as RNA immunoprecipitation, RNA pull-down, and ChIP sequencing revealed and verified the molecular mechanism by which LINC01305 recruits BNC1 to act on the GPS1 promoter to promote JNK phosphorylation and then mediate the epithelial–mesenchymal transition process of ESCC. Finally, clinical analysis revealed that BNC1 expression was elevated in moderately and poorly differentiated and lymph node metastatic ESCC tissues, which has the potential as a clinical diagnostic marker and targeted therapy.

Low methylation of ribosome biogenesis regulator 1 homolog (RRS1) promoter and its genomic gain may elevate RRS1 expression and predict poor prognosis for liver hepatocellular carcinoma (LIHC). Increased hsa-miR-132-3p expression may elevate RRS1 expression and result in poor prognosis for LIHC. Hsa-miR-132-3p inhibition can decrease RRS1 expression and the development of liver tumor cell lines.

Gilteritinib demonstrated significantly improved antitumor efficacy tha alectinib against ALK-rearranged NSCLC cells.

Deletion of FBXL5 results in the accumulation of intracellular ferrous iron, leading to cell cycle arrest and growth suppression in lung cancer.

In this study, we found that PI3K activation upregulated metabolic pathways that fine-tuned the cholesterol and steroid biogenesis. According to our data, the cholesterol synthesis pathway could constitute a metabolic vulnerability for PTEN-deficient cancers, and we speculate that this strategy has the potential to treat endocrine therapy-refractory breast and prostate cancers.

We show that Gln starvation triggers TGF-β-Smad2/3 signaling activation via class I HDAC activity and mTORC1 suppression in human mammary fibroblasts (HMFs), presumably inducing their phenotypic conversion to myofibroblastic CAFs (myCAFs) during tumor progression.

Mitochondria were increased in acquired GEM-resistant pancreatic cancer cell lines, which induced oxidative phosphorylation (OXPHOS) and upregulation of BCL2 and BCL-xL anti-apoptotic proteins. As a result of OXPHOS, the AMP/ATP ratio and AMP-activated protein kinase (AMPK) activity were decreased, which activated the heat shock factor 1 (HSF1)–heat shock protein (HSP) pathway to promote environmental stress tolerance.

The findings of this study demonstrate that specimens obtained through respiratory endoscopy are suitable for comprehensive genome profiling in the population including primary intrathoracic tumors and thoracic metastases of extrathoracic origin. In particular, medical thoracoscopy and conventional bronchoscopy involving cryobiopsy have proven to be useful, with suitability rates of 100% (18/18 cases) and 82.8% (24/29 cases), respectively.

Bevacizumab-resistant tumors secrete ESM1 to promote the high expression of DLL4 and MMP9, inducing tumor neovascularization and metastasis. Antagonism of ESM1 by monoclonal antibodies against ESM1 disrupts ESM1-DLL4/MMP9 signaling and enhances the antitumor efficacy of bevacizumab.

Using data from nationwide cancer registries, we showed the declining trends in newly diagnosed cervical cancer cases among Japanese women aged 20–29 years after the introduction of the HPV vaccination program; no similar trend was observed for older age groups. In addition, attribution of vaccine types HPV16 and HPV18 to invasive cervical cancer was reduced only among young women aged 20–29 years. This is the first report to suggest population-level effects of HPV vaccination on invasive cervical cancer in Japan.

We clarified for the first time that sperm-associated antigen 6 (SPAG6) is significantly upregulated in myeloproliferative neoplasm (MPN)-derived leukemia cells and regulated by signal transducer and activator of transcription 1 (STAT1), showing pro-oncogenic activity. Downregulation of SPAG6 could impair autocrine function of inflammatory cytokines, reduce reactivation of the JAK-STAT pathway, and sensitize interferon-α response through enhancing the induction level of STAT1 in MPN.

We analyzed the expression profile of esophageal squamous cell carcinoma before neoadjuvant chemotherapy and found that the immune-related expression profile was associated with the efficacy of the chemotherapy.