Abstract
Epigallocatechin-3-O-gallate (EGCG), a major polyphenol of green tea, has been shown to inhibit the growth of various cancer cell lines. We show here that EGCG induced the disruption of stress fibers and decreased the phosphorylation of the myosin II regulatory light chain (MRLC) at Thr18/Ser19, which is necessary for both contractile ring formation and cell division. Indirect immunofluorescence analysis revealed that EGCG inhibited the concentration of both F-actin and the phosphorylated MRLC in the cleavage furrow at the equator of dividing cells. In addition, EGCG increased the percentages of cells in the G2/M phase and inhibited cell growth. Recently, we have demonstrated that the anticancer activity of EGCG is mediated by the metastasis-associated 67 kDa laminin receptor (67LR). To explore whether the effect of EGCG is mediated by the 67LR, we transfected cells with short hairpin RNA (shRNA) expression vector to downregulate 67LR expression. When the 67LR was silenced, the suppressive effect of EGCG on the MRLC phosphorylation was significantly attenuated. These results suggest that EGCG inhibits the cell growth by reducing the MRLC phosphorylation and this effect is mediated by the 67LR.
| Original language | English |
|---|---|
| Pages (from-to) | 628-635 |
| Number of pages | 8 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 333 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Jul 29 2005 |
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All Science Journal Classification (ASJC) codes
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
Cite this
Epigallocatechin-3-O-gallate disrupts stress fibers and the contractile ring by reducing myosin regulatory light chain phosphorylation mediated through the target molecule 67 kDa laminin receptor. / Umeda, Daisuke; Tachibana, Hirofumi; Yamada, Koji.
In: Biochemical and Biophysical Research Communications, Vol. 333, No. 2, 29.07.2005, p. 628-635.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Epigallocatechin-3-O-gallate disrupts stress fibers and the contractile ring by reducing myosin regulatory light chain phosphorylation mediated through the target molecule 67 kDa laminin receptor
AU - Umeda, Daisuke
AU - Tachibana, Hirofumi
AU - Yamada, Koji
PY - 2005/7/29
Y1 - 2005/7/29
N2 - Epigallocatechin-3-O-gallate (EGCG), a major polyphenol of green tea, has been shown to inhibit the growth of various cancer cell lines. We show here that EGCG induced the disruption of stress fibers and decreased the phosphorylation of the myosin II regulatory light chain (MRLC) at Thr18/Ser19, which is necessary for both contractile ring formation and cell division. Indirect immunofluorescence analysis revealed that EGCG inhibited the concentration of both F-actin and the phosphorylated MRLC in the cleavage furrow at the equator of dividing cells. In addition, EGCG increased the percentages of cells in the G2/M phase and inhibited cell growth. Recently, we have demonstrated that the anticancer activity of EGCG is mediated by the metastasis-associated 67 kDa laminin receptor (67LR). To explore whether the effect of EGCG is mediated by the 67LR, we transfected cells with short hairpin RNA (shRNA) expression vector to downregulate 67LR expression. When the 67LR was silenced, the suppressive effect of EGCG on the MRLC phosphorylation was significantly attenuated. These results suggest that EGCG inhibits the cell growth by reducing the MRLC phosphorylation and this effect is mediated by the 67LR.
AB - Epigallocatechin-3-O-gallate (EGCG), a major polyphenol of green tea, has been shown to inhibit the growth of various cancer cell lines. We show here that EGCG induced the disruption of stress fibers and decreased the phosphorylation of the myosin II regulatory light chain (MRLC) at Thr18/Ser19, which is necessary for both contractile ring formation and cell division. Indirect immunofluorescence analysis revealed that EGCG inhibited the concentration of both F-actin and the phosphorylated MRLC in the cleavage furrow at the equator of dividing cells. In addition, EGCG increased the percentages of cells in the G2/M phase and inhibited cell growth. Recently, we have demonstrated that the anticancer activity of EGCG is mediated by the metastasis-associated 67 kDa laminin receptor (67LR). To explore whether the effect of EGCG is mediated by the 67LR, we transfected cells with short hairpin RNA (shRNA) expression vector to downregulate 67LR expression. When the 67LR was silenced, the suppressive effect of EGCG on the MRLC phosphorylation was significantly attenuated. These results suggest that EGCG inhibits the cell growth by reducing the MRLC phosphorylation and this effect is mediated by the 67LR.
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UR - http://www.scopus.com/inward/citedby.url?scp=20544461621&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2005.05.108
DO - 10.1016/j.bbrc.2005.05.108
M3 - Article
C2 - 15946647
AN - SCOPUS:20544461621
VL - 333
SP - 628
EP - 635
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -