Wu J.-M.Chen Y.Chen J.-C.Lin T.-Y.SHENG-HONG TSENG2020-03-122020-03-1220100304-3835https://www.scopus.com/inward/record.uri?eid=2-s2.0-72949109102&doi=10.1016%2fj.canlet.2009.06.009&partnerID=40&md5=4e58d7fdda6959ffbcd85f08800a5fa4https://scholars.lib.ntu.edu.tw/handle/123456789/476161Tetrandrine, a bisbenzylisoquinoline alkaloid, exerts antitumor effects against some cancers. We explored tetrandrine's effects on colon cancer with cultured mouse CT-26 cells and with subcutaneous tumors. Tetrandrine induced apoptosis in concentration- and time-dependent manner. Tetrandrine increased expression of ERK 1/2 and p38 MAPK; inhibition of p38 MAPK reduced tetrandrine-induced apoptosis; inhibition of ERK1/2 did not. Tetrandrine had significant effects on tumors including slower growth and longer animal survival time and higher survival rate. Higher dose and earlier treatment were more effective than lower dose and delayed treatment. TUNEL staining showed prominent tetrandrine-induced apoptosis of tumors. These data suggest that tetrandrine induced significant apoptosis of cultured and subcutaneous CT-26 cells. Tetrandrine-induced apoptosis might be at least partially related to activation of the p38 MAPK signaling pathway. ? 2009 Elsevier Ireland Ltd. All rights reserved.Apoptosis; Colon cancer; Mitogen-activated protein kinase; Tetrandrine[SDGs]SDG3mitogen activated protein kinase 1; mitogen activated protein kinase 3; mitogen activated protein kinase p38; tetrandrine; animal cell; animal experiment; animal model; antineoplastic activity; apoptosis; article; cancer cell; cancer cell culture; cell proliferation; colon cancer; controlled study; dose response; drug dose comparison; growth inhibition; mouse; nick end labeling; nonhuman; nucleotide sequence; priority journal; protein expression; signal transduction; subcutaneous tissue tumor; survival rate; survival time; tumor growth; Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Benzylisoquinolines; Cell Line, Tumor; Cell Proliferation; Cell Survival; Colonic Neoplasms; Dose-Response Relationship, Drug; In Situ Nick-End Labeling; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; p38 Mitogen-Activated Protein Kinases; Protein Kinase Inhibitors; Signal Transduction; Time Factors; Tumor Burden; Animalia; Musjournal article10.1016/j.canlet.2009.06.009195867122-s2.0-72949109102