RBM15 (RNA Binding Motif Protein 15)

This RBM15-USP10-NRF2 axis drives resistance to cisplatin and 5-fluorouracil (5-FU) both in vitro and in vivo. Disruption of this pathway sensitizes GC cells to chemotherapy and suppresses tumour growth. Collectively, our findings suggest that RBM15 is both a predictive biomarker and a therapeutic target for overcoming chemotherapy resistance in GC cells.

The bindings of circFGFR3 to EIF4A3 and EIF4A3 to JAK2, STAT3, or STAT5 were analyzed. In conclusion, RBM15 promotes PD-L1-mediated immune escape and accelerates OC progression by upregulating circFGFR3 expression through m6A modification and activating the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.

In-depth studies have revealed that RBM15 affects the progression of various diseases by regulating the expression of multiple genes, and its m6A methylation modification process is also considered to be an effective therapeutic target. In this paper, we review the latest research progress on the regulation of m6A methylation modification of RBM15, its molecular regulation in various diseases, such as cancer and metabolic diseases, and the potential therapeutic drugs derived from it, with a view to providing therapeutic strategies for the subsequent research on RBM15 and gene therapy targeting RBM15.

Overexpression of RBM15B or KDM4C attenuated ferroptosis and reversed the suppression of HCC cell growth induced by FOXP2 overexpression. In conclusion, FOXP2 may promote ferroptosis and inhibit cell proliferation in HCC by decreasing SLC7A11 expression via the RBM15B/KDM4C axis in an m6A-dependent manner.

However, overexpression of FTH1 suppressed ferroptosis and promoted tumor growth. Taken together, PRMT5/RBM15/ferritinophagy signaling can be a potential target for HCC.

Since the origin, significance and impact of many fusion transcripts remain unknown, our results support using an unbiased approach to identify fusion transcripts. This will help us to fully comprehend the complexity of the human transcriptome in normal biology and in disease.

Furthermore, animal and patient-derived organoid models revealed that RBM15 enhances the sensitivity of GC to 5-fluorouracil (5-FU) chemotherapy in an ECT2-dependent manner. In conclusion, this study defines a novel RBM15/IGF2BP3-ECT2 signaling axis that regulates EMT and chemosensitivity in GC via m6A methylation, providing both mechanistic insights and a potential therapeutic strategy.

We further demonstrate that blockade of the H3K79me2-RBM15B-m6A axis inhibits the survival of leukemia cells and promotes cell differentiation, and impairs hematological malignancies. This study uncovers a novel selective m6A deposition mechanism mediated by H3K79me2 and RBM15B, highlighting promising therapeutic targets for hematological malignancies.

In addition, knocking down RBM15 effectively reversed the effects of Rum mentioned above in vivo and in vitro. Mechanistically, Rum activates the NLRP3/ASC/Caspase-1 axis-mediated pyroptotic signaling in PTC by upregulating RBM15 to increase the N6-methyladenosine methylation modulation of NLRP3, thereby providing a novel strategy and target for the clinical treatment of PTC.

Collectively, our findings demonstrate that RBM15 stabilizes PFKFB4 expression in BC through an m6A-IGF2BP3-dependent mechanism and thus promotes the glycolysis and inhibits CD8+ T cell function. Targeting RBM15 sensitizes tumors to PD1 blockade and provides a promising therapeutic strategy for BC.

Due to their diagnostic, prognostic and predictive value, m6A regulators have emerged as promising biomarkers in gynaecological cancers in recent years. This review highlights the role of m6A regulators and critically evaluates their biomarker and clinical potential in gynaecological cancers.

This discovery furnished compelling experimental evidence supporting the clinical utility of ASIV in combating CRC metastasis. Significantly, our research underscored the substantial advantages of targeting exosome-mediated metastasis, thereby highlighting the necessity for subsequent clinical validation.