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Lycopene suppressed leptin‐mediated malignant progression in human colon cancer cells
Author(s) -
Lin MengChiu,
Tang FengYao
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.720.12
Subject(s) - colorectal cancer , cancer research , cancer , leptin , epithelial–mesenchymal transition , cancer cell , signal transduction , medicine , metastasis , endocrinology , biology , microbiology and biotechnology , obesity
Colorectal cancer is one of the leading causes of cancer death in western countries. Previous studies indicate that leptin induces cellular proliferation through multiple signalling pathways in colon cancer cells. Recent studies suggested that loss of E‐cadherin adherent molecule has been associated with epithelial–mesenchymal transition (EMT) and the malignant progression of human colon cancer cells. Our previous studies indicated that lycopene could exhibit anti‐cancer effects on human colon cancer cells. However, the inhibitory effect of lycopene on leptin‐mediated malignant progression of human colon cancer has not been demonstrated well yet. The present study demonstrated that leptin dose‐dependently (0, 0.0125, 0.0625, 0.25μM) induced cellular migration and invasion through up‐regulation of matrix metalloproteinase (MMP)‐7 as well as suppression of E‐cadherin in human colon cancer HT‐29 cells. The molecular mechanisms of actions were through the modulation of MAPK/JNK and JAK/STAT‐3 signaling pathways. Furthermore, our results demonstrated that lycopene (2 μM) effectively inhibited leptin‐mediated cellular migration through up‐regulation of E‐cadherin molecule and modulation of JNK signaling pathway in human colon cancer HT‐29 cells. Take together; our results suggest that lycopene could act as an effective chemo‐preventive agent against the leptin‐ mediated malignant progression in human colon cancer cells. Grant Funding Source : National Science Council grant under agreement No. 97‐2320‐B‐039‐043‐MY3