title: Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells.
abstract: Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients. The Chinese herb, Isodon eriocalyx, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from I. eriocalyx, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future.
authors.affiliation: Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.|Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Public Health, Jinan, 250012, Shandong, People's Republic of China.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
authors.forename: Zhijie
authors.initials: Z
authors.lastname: Xu
authors.affiliation: Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.|Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Public Health, Jinan, 250012, Shandong, People's Republic of China.
authors.forename: Zhengchuan
authors.initials: Z
authors.lastname: Niu
authors.affiliation: Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China.|Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Public Health, Jinan, 250012, Shandong, People's Republic of China.
authors.forename: Benjia
authors.initials: B
authors.lastname: Liang
authors.affiliation: Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, People's Republic of China. niujun100@126.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Niu
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D018938:Caco-2 Cells; D053148:Caspase 3 / Q000378:metabolism; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology; D053938:DNA Fragmentation / Q000187:drug effects; D004224:Diterpenes / Q000737:chemistry / Q000633:toxicity*; D015536:Down-Regulation / Q000187:drug effects; D006801:Humans; D037602:Isodon / Q000737:chemistry / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D004224:Diterpenes; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; C000613555:epieriocalyxin A; D048031:JNK Mitogen-Activated Protein Kinases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D053148:Caspase 3
keywords: Cell apoptosis; Colorectal cancer; Epieriocalyxin A; Signaling pathway