Compound C Inhibits B16-F1 Tumor Growth in a Syngeneic Mouse Model Via the Blockage of Cell Cycle Progression and Angiogenesis.

ABSTRACT: We recently observed that Compound C (CompC), a reversible inhibitor of AMP-activated protein kinase, reduced the cell viability of B16-F1 melanoma cells. To establish its molecular mechanism(s) of action, the cell cycle was examined by flow cytometry and the expression of cell cycle regulatory proteins and angiogenesis-related proteins were examined by western blot analysis. In addition, its effect on tumor growth was investigated using C57BL/6 syngeneic mice bearing B16-F1 xenografts. We found that CompC induced G2/M cell cycle arrest, which was associated with reduced levels of cell cycle regulatory proteins, such as phosphorylated pRB, cyclin-dependent protein kinases (Cdks), cyclins, and phosphorylated P-Ser10-histone H3, and increased levels of Cdk inhibitors, such as p21 and p53. We

SUBMITTER: Lee YT 

PROVIDER: S-EPMC6627246 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature