Inhibition of Growth and Survival of Head and Neck Cancer Cells by Silibinin Involves the Down-Regulation of Erk1/2, AKT and STAT3 Signaling.

Head and neck squamous cell carcinoma (HNSCC) is one of the most prevalent and fatal cancers in India. Silibinin, a naturally occurring small molecule from milk thistle (Silybum marianum), is gaining attention as a potent anticancer agent against various cancers; however, its impact on HNSCC and the associated molecular mechanisms are largely unknown. We checked the effect of silibinin on proliferation, cell viability, and DNA damage in HNSCC cells, and employed immunoblotting to detect the underlined molecular mechanism.

miR-24-2 targets Akt and inhibits cell survival, EMT, and tumour growth in triple-negative breast cancer.

Background: Breast cancer is one of the most common types of cancer in the world, and triple-negative breast cancer (TNBC) is an extremely aggressive subtype. This study aimed to investigate the efficacy and mechanisms of miR-24-2 against TNBC.

Methods: MDA-MB-231 (TNBC), HEK293T and HEK293 cells were used for various assays including cell viability and proliferation, cell migration, and invasion.

Silymarin prevents endothelial dysfunction by upregulating Erk-5 in oxidized LDL exposed endothelial cells.

Extracellular signal-regulated kinase (Erk)-5 is a key mediator of endothelial cell homeostasis, and its inhibition causes loss of critical endothelial markers leading to endothelial dysfunction (ED). Circulating oxidized low-density lipoprotein (oxLDL) has been identified as an underlying cause of ED and atherosclerosis in metabolic disorders. Silymarin (Sym), a flavonolignan, possesses various pharmacological activities however its preventive mechanism in ED warrants further investigation.

EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways.

Aim: To study the role of EGFR signaling in regulation of intrinsic resistance in prostate cancer.

Materials And Methods: Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, growth kinetics, colony formation, transwell migration, invasion and trypan blue assays along with inhibitors erlotinib, NU7441, B02, PD98059 and LY294002 were used.