RBM6 (RNA Binding Motif Protein 6)

Thus, under normal conditions, RBM6 promotes prostate tumour cell migration, but in the context of high ZEB1 expression, it inhibits migration. This shift in RBM6's regulatory capacity towards downstream genes underscores the importance of considering objective conditions in studying RBM6 molecules.

Furthermore, the immunotherapy response and drug sensitivity were all higher than that in low-risk groups (P < 0.05). A five-gene prognosis risk model which exhibit promising predictive ability in survival is constructed for patients with PAAD.

These genes play significant roles in the PI3K-Akt pathway and potentially interact with vitamin D. Molecular docking and single-cell RNA sequencing analyses suggest that vitamin D may improve the prognosis of glioma patients infected with COVID-19 by regulating these key genes and the PI3K-Akt pathway. The findings reveal molecular links between glioma and COVID-19, thereby providing new insights for developing targeted therapeutic strategies.

In summary, our study highlights the important role of RBM6, as well as the downstream targets and regulated pathways, suggesting the potential regulatory mechanisms of RBM6 in the development of cancer.

These included splicing factor 1 (SF1; median and IQR for GS=7: 4.6, 3.3-7.4; p=5.60E-03; q=0.04), uroplakin 3B-like (UPK3BL; median and IQR for GS=7: 7.4, 5.5-9.3; p=7.20E-03; q= 0.04), and RNA binding motif protein 6 (RBM6; median and IQR for GS=7: 10.3, 8.9-12.1; p=0.01; q=0.05). While replication is needed, these findings add to growing evidence that RNA expression differences in prostate tumors by race or ancestry may contribute to prostate tumor aggressiveness and prostate cancer disparities.

Accordingly, RBM6-deficient cancer cells are vulnerable to ATM and PARP inhibition and show remarkable sensitivity to cisplatin...Furthermore, we observe that RBM6 protein is significantly lost in metastatic breast tumors compared with primary tumors, thus suggesting RBM6 as a potential therapeutic target of advanced breast cancer. Collectively, our results elucidate the link between the multifaceted roles of RBM6 in regulating alternative splicing and HR of DSBs that may contribute to tumorigenesis, and pave the way for new avenues of therapy for RBM6-deficient tumors.