RBMS2 (RNA Binding Motif Single Stranded Interacting Protein 2)

Our findings indicate that RBMS2 inhibits CRC progression by promoting ferroptosis and regulating SLC7A11 mRNA stability. Targeting the RBMS2-SLC7A11 axis could provide a novel therapeutic strategy for CRC.

The LINC01094-miR-128-3p-RUNX1 feedback loop downregulates CDKN1A and promotes GC cooperatively with RBMS2 and HDAC1. Furthermore, Ro 5-3335 may hold promising therapeutic potential in the treatment of GC. Hence, our study found an oncogenic lncRNA, LINC01094, which could be a promising target for cancer treatment and diagnosis.

Validation through immunodetection techniques confirmed high expression of CD44 and CD63, two known drug resistance mediators with elevated proteomics expression results. The information revealed by the sensitivity of this method warrants it as an important tool for elaborating the complexity of acquired drug resistance in CRC.

Additionally, our research has unearthed links between RBMS2 and immune infiltration within the ccRCC tumor microenvironment. Collectively, our results underscore the tumor-inhibiting role of RBMS2 in ccRCC and spotlight its potential as a prognostic marker and therapeutic intervention target.

In conclusion, our study identified the molecular targets of PCMT1 in the TNBC cell line, expands our understanding of the regulatory mechanisms of PCMT1 in cancer progression, and provides novel insights into the progression of TNBC. The identified molecular targets are potential therapeutic targets for future TNBC treatment.

RBMS2 positively regulated BMF expression and increased BMF-induced expression of (cleaved) caspase 3, (cleaved) caspase 9 and poly (ADP-Ribose) polymerase (PARP). These results uncovered a novel mechanism for RBMS2 in the sensibilization of doxorubicin, suggesting that RBMS2 may act as a potential therapeutic target for drug-resistant breast cancer.