TitleThe dietary phytochemical chlorophyllin alters E-cadherin and beta-catenin expression in human colon cancer cells.
Publication TypeJournal Article
Year of Publication2004
AuthorsCarter O, Bailey GS, Dashwood RH
JournalJ Nutr
Volume134
Issue12 Suppl
Pagination3441S-3444S
Date Published2004 12
ISSN0022-3166
Keywordsbeta Catenin, Biomarkers, Cadherins, Cell Differentiation, Cell Nucleus, Chlorophyllides, Colonic Neoplasms, Cytoskeletal Proteins, Gene Expression, Humans, Immunohistochemistry, Microscopy, Confocal, RNA, Messenger, Trans-Activators, Tumor Cells, Cultured
Abstract

Chlorophyllin (CHL), an anticarcinogenic and antimutagenic water-soluble derivative of chlorophyll, has been reported to induce apoptosis in human colon cancer cells via a pathway involving cell differentiation. Induction of differentiation markers may be important in limiting cancer-cell invasion and metastasis, and there is much interest in understanding the underlying mechanisms, because this might provide insights for cancer chemotherapy. In the present study, human HCT116 colon-cancer cells were treated with CHL, and the expression levels of E-cadherin and beta-catenin were examined using immunocytochemistry and laser scanning confocal microscopy. E-cadherin was detected almost exclusively at the cell periphery of cancer cells treated with or without CHL, but the expression of E-cadherin in the plasma membrane was markedly elevated in the cells treated with CHL. beta-Catenin also was strongly expressed in the plasma membrane, especially after CHL treatment. No change in the expression of beta-catenin mRNA was detected across a broad range of CHL concentrations (10-500 micromol/L), but there was a concentration-dependent decrease in nuclear beta-catenin protein levels without overt changes in the cytosolic pool of beta-catenin. Our interpretation of these findings is that CHL induces E-cadherin expression, and this facilitates trafficking of beta-catenin away from the nucleus and into the plasma membrane, possibly for destruction via the adherins junction remodeling (Hakai) pathway.

DOI10.1093/jn/134.12.3441S
Alternate JournalJ. Nutr.
PubMed ID15570051
PubMed Central IDPMC2478518
Grant ListR01 CA080176-03 / CA / NCI NIH HHS / United States
P01 CA090890 / CA / NCI NIH HHS / United States
P01 CA090890-01A20003 / CA / NCI NIH HHS / United States
P30 ES00210 / ES / NIEHS NIH HHS / United States
R01 CA080176 / CA / NCI NIH HHS / United States
P01 CA090890-05S1 / CA / NCI NIH HHS / United States
CA80176 / CA / NCI NIH HHS / United States
R29 CA065525 / CA / NCI NIH HHS / United States
P01 CA090890-05 / CA / NCI NIH HHS / United States
R01 CA065525 / CA / NCI NIH HHS / United States
R01 CA065525-08 / CA / NCI NIH HHS / United States
R01 CA080176-02 / CA / NCI NIH HHS / United States
R01 CA065525-09 / CA / NCI NIH HHS / United States
T32 ES07060 / ES / NIEHS NIH HHS / United States
R01 CA080176-05 / CA / NCI NIH HHS / United States
CA65525 / CA / NCI NIH HHS / United States
R01 CA065525-07 / CA / NCI NIH HHS / United States
R01 CA080176-04 / CA / NCI NIH HHS / United States
R01 CA065525-06A1 / CA / NCI NIH HHS / United States
P01 CA090890-01A29001 / CA / NCI NIH HHS / United States
T32 ES007060 / ES / NIEHS NIH HHS / United States
P30 ES000210 / ES / NIEHS NIH HHS / United States