title: Scutellarin suppresses growth and causes apoptosis of human colorectal cancer cells by regulating the p53 pathway.
abstract: Scutellarin is a flavonoid isolated from a medicinal herb Scutellaria barbata D. Don and exerts therapeutic effects on cardiovascular diseases. However, it remains unclear whether Scutellarin exhibits anti‑tumor actions on human colon cancer. The current study aimed to investigate whether Scutellarin produces antiproliferative and pro‑apoptotic effects on HCT‑116 human colon cancer cells and to elucidate the mechanisms involved. Human colon cancer cells were exposed to different concentrations of Scutellarin, and cellular growth and apoptosis were evaluated by MTT assay, terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling (TUNEL) staining, western blot analysis and other assays. A cell viability assay demonstrated that Scutellarin treatment reduced the viability of HCT‑116 cells in a dose‑ and time‑dependent manner. TUNEL staining demonstrated that Scutellarin also induced apoptotic changes in HCT‑116 cells. The expression level of the anti‑apoptotic protein, Bcl‑2 apoptosis regulator (Bcl‑2), was reduced by Scutellarin in HCT‑116 cells, whereas the expression Bcl‑2 associated X apoptosis regulator (Bax) and the activation of caspase‑3 protein were increased by Scutellarin treatment. Further investigation revealed that Scutellarin significantly increased the phosphorylation of p53 protein in HCT‑116 cells. Additionally, suppression of p53 using a specific inhibitor, pifithrin‑α, abrogated the pro‑apoptotic effects of Scutellarin in HCT‑116 cells. Collectively, Scutellarin reduced the viability and induced apoptosis of human colon carcinoma cells, potentially by regulating p53 and Bcl‑2/Bax expression. These data suggested that Scutellarin may be useful as a promising anti‑tumor drug for treating colon cancer.
authors.affiliation: Department of Oncology, The Affiliated Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
authors.forename: Ning
authors.initials: N
authors.lastname: Yang
authors.affiliation: Department of Oncology, The Affiliated Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
authors.forename: Yuying
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Oncology, The Affiliated Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
authors.forename: Zhipeng
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Clinical and Laboratory Medicine, The Affiliated Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Gastrointestinal Oncology, The Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150040, P.R. China.
authors.forename: Yanqiao
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000737:chemistry / Q000494:pharmacology*; D047310:Apigenin / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005965:Glucuronates / Q000737:chemistry / Q000494:pharmacology*; D045325:HCT116 Cells; D006801:Humans; D012007:Rectum / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D031363:Scutellaria / Q000737:chemistry; D015398:Signal Transduction / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D005965:Glucuronates; D016159:Tumor Suppressor Protein p53; C484876:scutellarin; D047310:Apigenin