title: Carvacrol inhibits proliferation and induces apoptosis in human colon cancer cells.
abstract: Colon cancer is one of the most common malignancies worldwide and has a high mortality rate. Carvacrol is a major component of oregano and thyme essential oils and shows antitumor properties. Here, we investigated the effects of carvacrol on the proliferation and apoptosis of two human colon cancer cell lines, HCT116 and LoVo, and studied the molecular mechanisms of its antitumor properties. We found that carvacrol inhibited the proliferation and migration of the two colon cancer cell lines in a concentration-dependent manner. Cell invasion was suppressed after carvacrol treatment by decreasing the expression of matrix metalloprotease-2 (MMP-2) and MMP-9. Carvacrol treatment also caused cell cycle arrest in the G2/M phase and decreased cyclin B1 expression. Finally, carvacrol induced cell apoptosis in a dose-dependent manner. At the molecular level, carvacrol downregulated the expression of Bcl-2 and induced the phosphorylation of the extracellular-regulated protein kinase and protein kinase B (p-Akt). In parallel, carvacrol upregulated the expression of Bax and c-Jun N-terminal kinase. These results indicate that carvacrol might induce apoptosis in colon cancer cells through the mitochondrial apoptotic pathway and the MAPK and PI3K/Akt signaling pathways. Together, our results suggest that carvacrol may have therapeutic potential for the prevention and treatment of colon cancer.
authors.affiliation: Departments of aPathophysiology bPathology and cPharmacology, Harbin Medical University-Daqing dDepartment of Surgery, Fifth Clinical College of Harbin Medical University, Daqing, Heilongjiang, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Fan
authors.forename: Xiaolei
authors.initials: X
authors.lastname: Li
authors.forename: Yonggang
authors.initials: Y
authors.lastname: Cao
authors.forename: Hanping
authors.initials: H
authors.lastname: Qi
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.forename: Qianhui
authors.initials: Q
authors.lastname: Zhang
authors.forename: Hongli
authors.initials: H
authors.lastname: Sun
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D003110:Colonic Neoplasms; D000081007:Cymenes; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D039821:Monoterpenes / Q000494:pharmacology*; D009361:Neoplasm Invasiveness; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D000081007:Cymenes; D039821:Monoterpenes; D019253:Proto-Oncogene Proteins c-bcl-2; C073316:carvacrol; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases