Evaluation of CHK1 activation in vulvar squamous cell carcinoma and its potential as a therapeutic target in vitro.

CHK1 is an important regulator of the cell cycle and DNA damage response, and its altered expression has been identified in various tumors. Chk1 inhibitors are currently being evaluated as monotherapy and as potentiators of chemotherapy in clinical settings. However, to our knowledge, no previous study has investigated either the activation status or the therapeutic potential of CHK1 targeting in vulvar cancer.

MtDNA depletion influences the transition of CD44 subtypes in human prostate cancer DU145 cells.

Our earlier study revealed that long-term ethidium bromide application causes mitochondrial DNA depletion in human prostate cancer DU145 cell line (DU145), and this DU145 subline appears to have expanded CD44 cell population than its parental wild type DU145 cells (DU145). Increasing evidence suggests that CD44 cells are highly cancer stem cell like, but it is not clear about their dynamic transition between CD44 and CD44 phenotypes in prostate cancer cells, and how it is affected by mitochondrial DNA depletion. To address these questions, four cell subpopulations were isolated from both DU145 and DU145 cell lines based on their CD44 expression level and mitochondrial membrane potential.

Metabolic reprogramming is associated with flavopiridol resistance in prostate cancer DU145 cells.

Flavopiridol (FP) is a pan-cyclin dependent kinase inhibitor, which shows strong efficacy in inducing cancer cell apoptosis. Although FP is potent against most cancer cells in vitro, unfortunately it proved less efficacious in clinical trials in various aggressive cancers. To date, the molecular mechanisms of the FP resistance are mostly unknown.