SMARCA5 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 5)

The activity of SMARCA5 is controlled spatiotemporally by transcription factor RUNX1, which only accumulates at sufficient levels with sustained MAPK signals. We further show that inhibition of the SMARCA5-containing NoRC complex specifically inhibits the growth of PDAC organoid but not that of normal tissue derived from patients.

The nanobiosensor exhibits a broad linear range from 10 fM to 100 nM, with a detection limit as low as 1.93 fM. Furthermore, in clinical validation experiments, the nanobiosensor successfully reveals the expression levels of cSMARCA5 in liver tissue and whole blood samples, from which hepatocellular carcinoma patients are accurately screened out among normal people, thereby providing a highly promising circulating RNA-based liquid biopsy tool with significant potential for clinical application.

Importantly, targeting the sPOM121/β-catenin axis in patient-derived pre-clinical and syngeneic mouse models halts prostate cancer aggressiveness and enhances anti-tumor immunity. Taken together, these findings reveal previously unknown actionable reprogramming functions of off-pore NUPs in solid tumors.

Furthermore, loss of Smarca5 in GCNPs in an established mouse model of SHH-MB results in prolonged survival of tumor bearing mice. Our data underline the critical role of SMARCA5 during the development of the cerebellum and the pathogenesis of SHH-MB.

The effect of METTL3 knockdown on SMARCA5 messenger RNA (mRNA) stability was evaluated using actinomycin D treatment...SMARCA5 upregulation reverted the si-METTL3-mediated inhibition of MTB-induced macrophage M1 polarization and inflammation (P < 0.05). METTL3-mediated SMARCA5 facilitates macrophage M1 polarization and inflammation, providing a novel target for TB treatment.

Mocetinostat and clofarabine offer valuable insights for the development of novel targeted therapies in neuroblastoma.

Our findings suggest that RIOK1 is a novel oncogenic driver that may serve as a potential diagnostic and therapeutic target for HCC.

Notably, disruption of SND1S426 phosphorylation impaired the SND1-SMARCA5 interaction, leading to significant inhibition of ESCC tumor growth and metastatic potential in vivo. Our findings unveil a novel mechanistic axis involving SND1 and SMARCA5 in chromatin remodeling and oncogenesis, offering promising therapeutic targets for ESCC intervention.

Depletion of USP3 or SMARCA5 promoted PCa cells sensitive to docetaxel and overexpression of USP3 restored the cells resistance to docetaxel treatment in SMARCA5 silenced cells in vitro and vivo. Clinically, USP3 was significantly up-regulated in prostate cancer tissues and positively associated with SMARCA5 expression. Collectively, our findings uncover a novel molecular mechanism for the USP3-SMARCA5 axis in regulating DSB repair with an important role in chemotherapy response in human prostate cancers, highlighting that targeting USP3-SMARCA5 axis could be a valuable strategy to treat USP3/SMARCA5-overexpressing chemotherapy-resistant patients and improve drug treatment.

Mechanistic studies have also shown that cpRNA promotes circRNA biogenesis, in part, by antagonizing the unwinding function of DHX9. Overall, these findings suggest that cpRNA represents a promising strategy for circRNA overexpression, offering a potential treatment for diseases marked by low circRNA levels.