RBMS3 (RNA Binding Motif Single Stranded Interacting Protein 3)

ISL1 serves as both a predictive biomarker and functional dependency, as evidenced by essentiality for cell survival and loss following treatment. Prospective studies using ISL1 as a predictive biomarker for lurbinectedin are planned.

ZEB1 interacted with the E-box motif in the GPX4 promoter, suppressing GPX4 transcription and thereby promoting ferroptosis. In conclusion, RBMS3-AS3, epigenetically downregulated by ALKBH5, facilitates LUAD progression by inhibiting ferroptosis via the HNRNPDL/ZEB1/GPX4 axis, and may serve as a novel therapeutic target for LUAD.

Despite the prominent oncogenic roles of multiple RBPs, RBP-targeting compounds aimed at suppressing VM in GBM have remained at an early stage due to a number of limitations. This review summarises the role of VM in the treatment resistance of GBM, RBP regulation of VM, and the current landscape and future direction of RBP-targeted therapies aimed at overcoming VM-mediated treatment resistance in GBM.

Using in vivo epistasis studies, we confirmed that RBMS3 regulation of TXNIP mRNA stability drives this metastasis-suppressive program. These findings position the RBMS3-TXNIP regulatory axis as a key post-transcriptional mechanism in breast cancer and illustrate how interpretable models of RNA dynamics can uncover hidden regulatory programs in disease.

These findings suggest that metformin, in combination with PD-L1 inhibitors, may enhance antitumor immune responses and improve treatment outcomes in OC. Targeting RBMS3 could represent a novel therapeutic approach for overcoming immune evasion in OC.

TIMER-based correlation analysis demonstrated a positive association between RBMS3 expression and immune cell infiltration, with the regression line indicating significant correlations for B cells (cor = 0.16, P = 4.25 × 10⁻4), CD8 + T cells (cor = 0.214, P = 1.86 × 10⁻⁶), CD4 + T cells (cor = 0.24, P = 8.99 × 10⁻⁸), macrophages (cor = 0.341, P = 1.07 × 10⁻14), neutrophils (cor = 0.277, P = 5.71 × 10⁻10), and dendritic cells (cor = 0.369, P = 3.70 × 10⁻17). These findings underscore RBMS3's dual role in LUAD as a tumor suppressor and immune microenvironment modulator, offering novel insights for prognosis and therapy.

These findings suggested that the CSF3R-AS/CSF3R/JAK2/STAT3 positive feedback loop could promote HCC progression and sorafenib resistance. Blocking this loop is expected to provide new research directions and therapy targets for HCC.

Importantly, the combination of ANGPT2 antibody in RBMS3-deficient HCC cells restores sensitivity to sorafenib both in vitro and in vivo. These findings uncovered a novel molecular basis for post-translational upregulation of ANGPT2, suggesting that RBMS3-loss plays an oncogenic role in HCC by promoting angiogenesis and conferring resistance to sorafenib treatment.

These results support that multiple altered regulatory mechanisms may contribute to the reduction of circRNA levels that characterize early colorectal carcinogenesis.

Our study introduces a novel diagnostic approach by identifying a panel of three mature miRNAs (hsa-miR-143-5p, hsa-miR-23b-3p, and hsa-miR-148b-3p) as novel and non-intrusive biomarkers for PC.

In vivo, metformin inhibited tumor growth, which was negated by RBMS3 silencing. Our findings suggest that metformin promotes ferroptosis and inhibits ovarian cancer progression by upregulating RBMS3, offering a promising direction for clinical application in ovarian cancer treatment.