CHEK1 overexpression

The overexpression of CHEK1 and PLK1 in TNBC compared to non-TNBC samples was validated by expression analysis. This study provides insights into the molecular mechanisms of TNBC and suggests CHEK1, PLK1, and their upstream regulators as potential therapeutic targets for TNBC treatment.

The current treatment regimen comprising surgical resectioning, chemotherapy with Temozolomide (TMZ), and adjuvant radiotherapy does not achieve total patient cure. We used in silico molecular docking to analyze and validate our objective to repurpose Dapagliflozin against CDK1/PBK/CHEK1. Our results showed that Dapagliflozin forms putative conventional hydrogen bonds with CDK1, PBK, and CHEK1 and arrests the cell cycle with the lowest energies as Abemaciclib.

MD simulations were performed for the selected protein-ligand complexes and the results were compared to the co-crystallised ligand, 3-(indol-2-yl)indazole. The results showed that compound INC000033832986 could be a natural alternative to the commercial ligand for the prevention of SCLC.Communicated by Ramaswamy H. Sarma.

Circ_0011292 could accelerate PTX resistance and cell malignant progression of NSCLC cells partially through the regulation of circ_0011292/miR-433-3p/CHEK1 axis.

The results indicated that the effects of miR-139-3p on the LUSC cell phenotypes could be blocked by overexpressing CHEK1. In conclusion, our study provides a novel insight into the regulatory role of miR-139-3p in the development of LUSC.

Cell clusters with CHEK1 expression were more prone to metastasis and epithelial-to-mesenchymal transition. CHEK1 might potentially act as a prognostic biomarker for LUAD.

Our findings suggest that targeting the enzymatic catalytic center encoded by CHEK1 mRNA and circCHEK1_246aa is a promising therapeutic modality to target both MM cells and BM niche.

Finally, in clinical samples, ovarian cancer patients with high levels of EZH2 and CHK1 not only were more resistant to platinum but also had a poorer prognosis. Our data revealed a previously unidentified functional and mechanistic link between EZH2 levels, CHK1 signaling activation, and ovarian CSCs and provided strong evidence that EZH2 promotes ovarian cancer chemoresistance and recurrence.