RBPMS (RNA-binding protein with multiple splicing)

And by down-regulating FDX1, we found that the expression level of genes involved in cuproptosis RS might be affected by FDX1 in THCA. Overall, our study identified a novel cuproptosis-based predictive model, and we demonstrated that cuproptosis is a promising therapeutic method for THCA, which enhances our understanding of the cuproptosis-related genes and provides valuable insights into the clinical treatment and molecular mechanisms of THCA.

Also, RNA-seq analyses indicated that while Sarm1 deficiency protected from IL1A+TNF induced RGC loss it did not significantly alter microglia and astrocyte responses. Altogether, these findings indicate that IL1A potentiates SARM1-dependent TNF-induced RGC death in vivo.

We identified nine target genes and propose a three-gene prognostic model for outcome prediction in PCa. Our findings suggest that targeting PLXNA4 may offer new therapeutic opportunities for the treatment of PCa, including immunotherapy.

Initial chemotherapy with the VAC regimen (vincristine, actinomycin D, and cyclophosphamide) was administered, but the response was poor. To our knowledge, this is the first reported case of infantile fibrosarcoma with RBPMS-NTRK3 fusion in China. Treatment with larotrectinib resulted in marked tumor shrinkage.

The TNBC prognostic signature comprising four interferon genes (STXBP1, LAMP3, CD276, and POLR2F) was identified, with their expression significantly correlated with the infiltration abundance of multiple immune cells and the drug sensitivity of 30 diverse drugs (ARQ-680, Fluphenazine, and Chelerythrine, etc.). In the prognostic signature and the ceRNA axes, STXBP1, RBPMS-AS1, and FAM198B-AS1 were first reported as potential biomarkers of TNBC. These findings have the potential to provide new insights into the mechanisms driving TNBC tumorigenesis and development.

Transcriptomic analysis of Fn14-overexpressing retinas in the ONC model further revealed significant downregulation of suppressor of cytokine signaling 3 (Socs3), a finding validated in both injury models. Our study highlights Fn14 as a key regulator of optic nerve injury, capable of enhancing RGC survival and axon regeneration.

The NLRP3 inhibitor MCC950 reversed these effects, confirming the involvement of this pathway. These findings suggest that RBPMS2 may be a potential therapeutic target for inducing pyroptosis in gastric cancer cells, providing novel insights into treatment strategies for gastric cancer.

Furthermore, ANKRD10-2 knockdown significantly rescued the migration enhancement induced by RBPMS depletion in BLCA cells. Taken together, this study revealed a mechanism whereby RBPMS suppresses the migration and invasion of BLCA cells by attenuating MYC pathway activity via the AS of ANKRD10.

Our case report strengthens the evidence that crizotinib may be a viable treatment option for patients with ICC with a c-MET tyrosine kinase fusion, necessitating additional clinical investigation.

As demonstrated in our PTC cohort, DNA CGP and RNA CGP may be complementary for fusion detection in certain tumor types. RNA CGP complements DNA CGP by detecting fusions that cannot be efficiently baited on DNA CGP, while DNA CGP may complement RNA CGP by detecting fusions in poor quality (e.g., old archival) samples when RNA sequencing may not be not technically feasible. Clinically relevant fusions detected in this retrospectively profiled PTC cohort included therapeutically targetable fusion events (e.g., RET, NTRK, ALK) and a PAX8::PPARG fusion, which is suggestive of a follicular variant PTC.

There also existed a targeting relationship and negative interplay between PLCL1 and miR-19a-3p. In short, RBPMS-AS1 sponges miR-19a-3p and represses the growth and EMT of CC cells via enhancing PLCL1-mediated pyroptosis.