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Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.625 5年インパクトファクター: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2013007522
pages 131-139

Luteolin Induces Growth Arrest in Colon Cancer Cells Through Involvement of Wnt/β-Catenin/GSK-3β Signaling

Ashok Kumar Pandurangan
Muthayammal Center for Advanced Research, Muthayammal College of Arts & Science, Rasipuram, Tamil Nadu, India; Department of Nutrition and Dietetics, Faculty of Medicine and Health Sciences, Universiti of Putra Malaya, Serdang, Selangor, Malaysia
Prakash Dharmalingam
Department of Biochemistry, Cell Biology Lab, University of Madras, Guindy Campus, Chennai, India
Suresh Kumar Ananda Sadagopan
Department of Biochemistry, Cell Biology Lab, University of Madras, Guindy Campus, Chennai, India
Manikandan Ramar
Department of Zoology, University of Madras, Guindy Campus, Chennai, India
Arumugam Munusamy
Department of Zoology, University of Madras, Guindy Campus, Chennai, India
Ashok Kumar Pandurangan
School of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and Technology, Vandalur, Chennai, Tamil Nadu, India 600048

要約

Cancer is a multistep process that typically occurrs over an extended period of time, beginning with initiation followed by promotion and progression. Colon cancer is the leading cause of morbidity and mortality worldwide. For a variety of reasons, patients prefer naturally occurring dietary substances over synthetic agents to prevent cancer. Luteolin, a bioflavonoid, possesses antioxidant, anti-inflammatory, and antiproliferative effects. We analyzed the in vitro anticancer and apoptosis-inducing property of luteolin using HCT-15 colon adenocarcinoma cells. Cell viability was assessed using trypan blue assay at different concentrations. Luteolin at a concentration of 100µM (IC50) decreased the expressions of non-P-β-catenin, phosphorylated (inactive) glycogen synthase kinase-3β, and cyclin D1 expressions in HCT-15 cells, which were confirmed by Western blot analysis. Luteolin also promoted substantial cell cycle arrest at the G2/M phase in HCT-15 cells, and it induces apoptosis in HCT-15 cells, as revealed by flow cytometric analysis. Furthermore, Western blot analysis showed that luteolin treatment enhanced the expression of Bax and caspase-3, whereas the expression of Bcl-2 was suppressed. Together, the results of this study revealed that luteolin can act as a potent inhibitor of HCT-15 proliferation and can be used as an agent against colon cancer.


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