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AMPK/p53 Axis Is Essential for α-Lipoic Acid–Regulated Metastasis in Human and Mouse Colon Cancer Cells
  1. Sunmi Park, BSc*,,
  2. Seung Kug Choi, BSc*,,
  3. Yura Choi, BSc*,†",
  4. Hyun-Seuk Moon, PhD*,,
  1. From the *Laboratory of Metabolic Engineering, Department of Biotechnology, College of Life Sciences and Biotechnology, †Institute of Animal Molecular Biotechnology, and ‡Biomedical Research Center of Guro Hospital, Research Driven Hospital, Korea University, Seoul, South Korea.
  1. Received July 2, 2015, and in revised form July 22, 2015.
  2. Accepted for publication July 23, 2015.
  3. Reprints: Hyun-Seuk Moon, PhD, Laboratory of Metabolic Engineering, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul, 136-713, South Korea, E-mail: mhs72{at}korea.ac.kr.
  4. Supported by grants from the Korea University (K1420781), Korea University Guro Hospital (O1500081), and Korea Institute of Oriental Medicine (R1508541).
  5. Conflict of Interest: The authors have declared no conflicts of interest.
  6. S.P. and H.S.M. participated in the study design, performance, and coordination. S.P., S.K.C., Y.C., and H.S.M. contributed to writing the manuscript. H.S.M. conceived the study. All authors read and approved the final article.

Abstract

α-Lipoic acid (ALA) has an anticancer property of lung, cervix, and prostate cancer cells. However, direct evidence that ALA contributes to the development of colon cancer has not been fully elucidated. In addition, no previous studies have evaluated whether ALA may regulate malignant potential, such as adhesion, invasion, and colony formation of colon cancer cells. To address the aforementioned questions, we conducted in vitro ALA signaling studies using human (HT29) and mouse (MCA38) colon cancer cell lines. We observed that cell proliferation is reduced by ALA administration in a dose-dependent manner in human and mouse colon cancer cell lines. Specifically, 0.5 to 1 mM concentration of ALA significantly decreased cell proliferation when compared with control. Similarly, we found that ALA downregulates adhesion, invasion, and colony formation. Finally, we observed that ALA activates p53 and AMPK signaling pathways in human and mouse colon cancer cells. We found for the first time that ALA suppresses cell proliferation and malignant potential via p53 and AMPK signaling pathways in human and mouse colon cancer cells. These new and early mechanistic studies provide a causal role of ALA in colon cancer, suggesting that ALA might be a useful agent in the management or chemoprevention of colon cancer.

Key Words
  • α-lipoic acid
  • colon cancer
  • cell proliferation
  • malignant potential
  • p53
  • AMPK

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