Open AccessMechanisms of Growth Inhibition of Human Lung Cancer Cell Line, PC‐9, by Tea Polyphenols
Author(s) -
Okabe Sachiko,
Suganuma Masami,
Hayashi Moriaki,
Sueoka Eisaburo,
Komori Atsumasa,
Fujiki Hirota
Publication year - 1997
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1997.tb00431.x
Subject(s) - growth inhibition , polyphenol , cell growth , cell culture , epigallocatechin gallate , cancer cell , cell cycle , biochemistry , genistein , mechanism of action , chemistry , cell , pharmacology , biology , cancer , in vitro , antioxidant , endocrinology , genetics
(–)‐Epigallocatechin gallate (EGCG), the main constituent of green tea, and green tea extract show growth inhibition of various cancer cell lines, such as lung, mammary, and stomach. We studied how tea polyphenols induce growth inhibition of cancer cells. Since green tea extract contains various tea polyphenols, such as EGCG, (–)‐epigallocatechin (EGC), (–)‐epicatechin gallate (ECG), and (–)‐epicatechin (EC), the inhibitory potential of each tea polyphenol on the growth of a human lung cancer cell line, PC‐9 cells, was first examined. EGC and ECG inhibited the growth of PC‐9 cells as potently as did EGCG, but EC did not show significant growth inhibition. The mechanism of growth inhibition by EGCG was studied in relation to cell cycle regulation. Flow cytometric analysis revealed that treatment with 50 μM and 100 μM EGCG increased the percentages of cells in the G 2 ‐M phase from 13.8% to 15.6% and 24.1%, respectively. The DNA histogram after treatment with 100 μM EGCG was similar to that after treatment with genistein, suggesting that EGCG induces G 2 ‐M arrest in PC‐9 cells. Moreover, we found by microautoradiography that [ 3 H]EGCG was incorporated into the cytosol, as well as the nuclei. These results provide new insights into the mechanisms of action of EGCG and green tea extract as cancer‐preventive agents in humans.