The molecular mechanism of <i>in vitro</i> anti-tumor effects of TMOC.

<p>(A) TMOC treatment inhibited the STAT3 phosphorylation and down-regulated the level of c-myc in a dose dependent manner. (B) A2780 and A2780/CDDP cells were transfected with STAT3 constitutively active (S3-CA) plasmid, STAT3 dominant negative (S3 DN) plasmid or control vector. (C) Introduction of S3-CA significant blocked the anti-proliferative activity of TMOC. In contrast, introduction of S3-DN sensitized the cancer cells to TMOC treatment. (D) TMOC inhibited the c-Src kinase phosphorylation and up-regulated the tumor surpressor PTEN in all of the three cell lines, but only up-regulated p53 in A2780 cells. β-actin was used as an equal loading control. The experiments were repeated three times and a representative experiment is shown. * <i>p</i><0.05, ** <i>p</i><0.01 compared to control.