Involvement of 67-kDa laminin receptor-mediated myosin phosphatase activation in antiproliferative effect of epigallocatechin-3-O-gallate at a physiological concentration on Caco-2 colon cancer cells

Daisuke Umeda, Satomi Yano, Koji Yamada, Hirofumi Tachibana

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33 Citations (Scopus)

Abstract

Previously we reported that 67-kDa laminin receptor (67LR) mediates epigallocatechin-3-O-gallate (EGCG)-induced cell growth inhibition and reduction of myosin regulatory light chain (MRLC) phosphorylation at Thr-18/Ser-19, which is important for cytokinesis. Here, we found that human colon adenocarcinoma Caco-2 cells exhibited higher expression level of 67LR and EGCG at a physiologically achievable concentration (1 μM) significantly accumulated the cells in G2/M phase without affecting expression of Wnt-signaling components. We also found that myosin phosphatase targeting subunit 1 (MYPT1) phosphorylation at Thr-696, which inhibits myosin phosphatase and promotes MRLC phosphorylation, was reduced in response to 1 μM EGCG. 67LR knockdown by RNA interference abolished the inhibitory effects of 1 μM EGCG on cell cycle progression and the phosphorylation of MRLC and MYPT1. These results suggest that through 67LR, EGCG at a physiological concentration can activate myosin phosphatase by reducing MYPT1 phosphorylation and that may be involved in EGCG-induced cell growth inhibition.

Original languageEnglish
Pages (from-to)172-176
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume371
Issue number1
DOIs
Publication statusPublished - Jun 20 2008
Externally publishedYes

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Myosin-Light-Chain Phosphatase
Laminin Receptors
Phosphorylation
Colonic Neoplasms
Chemical activation
Cells
Myosin Light Chains
Cell growth
Cytokinesis
Caco-2 Cells
G2 Phase
Growth
RNA Interference
Cell Division
epigallocatechin gallate
Cell Cycle
Colon
Adenocarcinoma
RNA

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "Previously we reported that 67-kDa laminin receptor (67LR) mediates epigallocatechin-3-O-gallate (EGCG)-induced cell growth inhibition and reduction of myosin regulatory light chain (MRLC) phosphorylation at Thr-18/Ser-19, which is important for cytokinesis. Here, we found that human colon adenocarcinoma Caco-2 cells exhibited higher expression level of 67LR and EGCG at a physiologically achievable concentration (1 μM) significantly accumulated the cells in G2/M phase without affecting expression of Wnt-signaling components. We also found that myosin phosphatase targeting subunit 1 (MYPT1) phosphorylation at Thr-696, which inhibits myosin phosphatase and promotes MRLC phosphorylation, was reduced in response to 1 μM EGCG. 67LR knockdown by RNA interference abolished the inhibitory effects of 1 μM EGCG on cell cycle progression and the phosphorylation of MRLC and MYPT1. These results suggest that through 67LR, EGCG at a physiological concentration can activate myosin phosphatase by reducing MYPT1 phosphorylation and that may be involved in EGCG-induced cell growth inhibition.",
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AU - Umeda, Daisuke

AU - Yano, Satomi

AU - Yamada, Koji

AU - Tachibana, Hirofumi

PY - 2008/6/20

Y1 - 2008/6/20

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AB - Previously we reported that 67-kDa laminin receptor (67LR) mediates epigallocatechin-3-O-gallate (EGCG)-induced cell growth inhibition and reduction of myosin regulatory light chain (MRLC) phosphorylation at Thr-18/Ser-19, which is important for cytokinesis. Here, we found that human colon adenocarcinoma Caco-2 cells exhibited higher expression level of 67LR and EGCG at a physiologically achievable concentration (1 μM) significantly accumulated the cells in G2/M phase without affecting expression of Wnt-signaling components. We also found that myosin phosphatase targeting subunit 1 (MYPT1) phosphorylation at Thr-696, which inhibits myosin phosphatase and promotes MRLC phosphorylation, was reduced in response to 1 μM EGCG. 67LR knockdown by RNA interference abolished the inhibitory effects of 1 μM EGCG on cell cycle progression and the phosphorylation of MRLC and MYPT1. These results suggest that through 67LR, EGCG at a physiological concentration can activate myosin phosphatase by reducing MYPT1 phosphorylation and that may be involved in EGCG-induced cell growth inhibition.

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