RBM8A (RNA Binding Motif Protein 8A)

Therapeutic targeting of this axis with the EGFR inhibitor gefitinib restored oxaliplatin sensitivity in vitro and synergistically suppressed RBM8A-driven xenograft growth in vivo. Additionally, single-cell RNA-seq revealed RBM8A enrichment in malignant gastric epithelial cells, while tissue microarrays confirmed that dual RBM8A/EGFR overexpression predicts the poorest survival outcomes. Collectively, our findings define the RBM8A-eIF4A3-EGFR axis as a druggable determinant of chemoresistance and establish RBM8A as both a prognostic biomarker and therapeutic target in GC.

This group demonstrated increased sensitivity to vincristine, etoposide, and oxaliplatin. Knockdown of PABPC4 significantly inhibited cell proliferation, reduced colony formation, and delayed tumor growth in vivo. The ERG scoring system offers a robust and precise tool for predicting survival and guiding personalized treatment in DLBCL patients.

Knockdown of RBM8A promoted RS of ANK3-TV4 and upregulated its expression. We investigate the role of RS in HCC, providing a novel therapeutic perspective and identifying potential targets for intervention.

Inhibition of Y14 phosphorylation interfered with Ku70/80 recruitment and increased the sensitivity of cancer cells to DNA damage. This study reinforces that manipulating DNA repair foci can improve the efficacy of anticancer agents.

Actinomycin D assays demonstrated that RBM8A promoted BBC3 mRNA degradation...In conclusion, RBM8A inhibited apoptosis and promoted GC progression by interacting with UPF3B, leading to degradation of the pro‑apoptotic gene BBC3 mRNA. These findings highlighted that interfering with RBM8A expression, or disrupting the interactions between RBM8A and BBC3 mRNA or between RBM8A and UPF3B could serve as potential therapeutic strategies for GC.

Collectively, these findings suggest that TEAD4 novel transcriptional target RBM8A interacts with EIF4A3 to increase IGF1R and IRS-2 expression and activate PI3K/AKT signaling pathway, thereby further promoting the malignant phenotype of BC cells.

This prognostic signature based on RBM family had a great value for predicting OS of HCC patients. Low-risk patients were more suitable for receiving immunotherapy and sorafenib treatment. The RBM family members made of the prognostic model might promote the progression of HCC.

Moreover, the silencing of RBM8A inhibited the growth of tumor xenograft in vivo. RBM8A knockdown may reduce DDP resistance in BC to repress the development of BC via the AKT/mTOR pathway, suggesting that RBM8A may serve as a new therapeutic target in BC.