tectoridin and Colonic-Neoplasms

Colon cancer is one of the most familiar malignancies worldwide, with high morbidity and high mortality. This study intended to explore the role and mechanism of tectoridin (TEC) in regulating the progression of colon cancer. First, colon cancer cell lines (HCT116 and SW480 cells) were treated with different doses of TEC (0-200 μM). Then, CCK8 and clone formation experiments were performed to detect cell proliferation. Flow cytometry and western blot were conducted to examine apoptosis. Subsequently, Transwell assay and wound-healing test was employed to determine the effect of TEC on colon cancer cell invasion and migration. Next, western blot was performed to monitor the PKC/p38 MAPK pathway activation. In addition, a tumor model was established in nude mice to explore the effect of TEC on tumor growth in vivo. TEC dose-dependently dampened the proliferation, migration and invasion of colon cancer cells and facilitated their apoptosis. In addition, TEC abated the tumor cell growth in vivo. Besides, TEC dose-dependently suppressed the expression of PKC and p38 MAPK. Moreover, inhibiting the PKC pathway almost cancel out the anti-tumor effects induced by TEC. TEC attenuates the colon cancer progression by inhibiting the PKC/p38 MAPK pathway.

Topics: Colonic Neoplasms; Down-Regulation; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; HCT116 Cells; Humans; Isoflavones; MAP Kinase Signaling System; Neoplasm Proteins; p38 Mitogen-Activated Protein Kinases; Protein Kinase C