BNC1 (Basonuclin 1)

Knockdown of BNC2 suppresses EMT, reduces invasiveness, and downregulates COL3A1, whereas COL3A1 overexpression rescues these effects, establishing the BNC2-COL3A1 axis as a critical driver of tumor progression. These findings highlight BNC2 as a potential biomarker and therapeutic target in pancreatic cancer, offering new insights into the molecular mechanisms underlying this aggressive disease.

HSF2BP significantly promotes LUAD progression by modulating the BNC1/TGF-β/SMAD3 signaling axis and reshaping the tumor immune microenvironment. Targeting the HSF2BP-BNC1 interaction can provide novel therapeutic strategies for enhancing immune responses against LUAD.

Importantly, proliferation can be blocked in SCC tumors using PRMT1 inhibitors, which has no effect on the repression of pro-migratory genes. Given the diverse gene expression programs regulated by transcription factors, this work demonstrates that pro-tumorigenic activities can be specifically targeted through the inhibition of co-factors without activating pathways that may lead to tumor progression.

Mechanistically, BNC1 suppresses CCL20 expression by binding to its promoter, leading to reduced activation of the JAK-STAT signaling pathway and promoting apoptosis in gastric cancer cells. These findings highlight the pivotal role of BNC1 in gastric cancer progression and suggest that targeting BNC1 and its downstream pathways could serve as a potential therapeutic strategy.

BNC1 protein interlinked with TCF21 protein, and bioluminescence imaging demonstrated that BNC1 enhanced TCF21 expression in the brain tissue of the mouse model of glioma. In conclusion, BNC1 reduced cell proliferation, and increased ferroptosis of glioma cells by TCF21/PI3K signaling pathway, may be a feasible strategy to treat glioma.

Excluding marginal zone and T-cell lymphomas, sensitivity increased to 84% (80%-88%). MDMs in plasma show promise to detect lymphoma and are candidates for inclusion in multi-cancer detection studies.

Our study highlights the clinical importance of BNC2 in MC, and targeting BNC2 on stromal cells (fibroblasts and endothelial cells) may be an effective strategy for treating MC.

Additionally, the METTL3 inhibitor STM2457 suppressed neoplastic phenotypes of arsenite-transformed BEAS-2B cells by blocking pri-miR-106b methylation. These results demonstrate that m6A modification promotes the neoplastic phenotypes of arsenite-transformed BEAS-2B cells through METTL3/miR-106b-5p/BNC2 pathway, providing a new prospective for understanding arsenic carcinogenesis.

Notably, cancer antigen 19-9 and carcinoembryonic antigen both had an accuracy of 90.0%. Our study suggests that analyzing seven differentially methylated genes with KRAS mutations in cfDNA using the novel Epi-TOP pancreatic assay is a potential blood-based biomarker for the diagnosis of PDAC.

A 4-fold increased prevalence of cancer was observed in men with genetic infertility compared to the general male population (8% vs. 2%; p = 4.4 × 10-3). Expanding genetic testing in andrology will contribute to the multidisciplinary management of SPGF.

We also revealed the molecular mechanism by which LINC01305 recruits BNC1 to the promoter of GPS1, and then GPS1 could mediate the JNK signaling pathway to promote the proliferation and metastases of ESCC. Taken together, we discovered the novel molecular mechanism by which LINC01305/BNC1 upregulates GPS1 expression to promote the development of ESCC, providing a new therapeutic target for ESCC.