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Growth‐inhibitory effect of quercetin and presence of type‐II estrogen‐binding sites in human colon‐cancer cell lines and primary colorectal tumors
Author(s) -
Ranelletti Franco O.,
Ricci Riccardo,
Larocca Luigi M.,
Maggiano Nicola,
Capelli Arnaldo,
Scambia Giovanni,
BenedettiPanici Pierluigi,
Mancuso Salvatore,
Rumi Carlo,
Piantelli Mauro
Publication year - 1992
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910500326
Subject(s) - cell growth , cell culture , in vivo , colorectal cancer , cell cycle , cell , cancer research , biology , chemistry , microbiology and biotechnology , cancer , medicine , biochemistry , genetics
Abstract We studied the effect of quercetin (Q) on the proliferation of HT‐29, WiDr, COLO 201, and LS‐174T human colon cancer cell lines. Q, between 10 nM and 10 μM, exerted a dose‐dependent, reversible inhibition of cell proliferation. Cell‐cycle analysis revealed that the growth‐inhibitory effect of Q was due to a blocking action in the G 0 /G 1 phase. Using a whole‐cell assay with 17β‐[ 3 H]‐estradiol as tracer, we demonstrated that all these cell lines contain type‐II estrogen‐binding sites (type‐II EBS). By using Q and other chemically related flavonols (3,7‐4′‐trimethox‐ yquercetin, 3,7,3,4′‐tetramethoxyquercetin, kaempferol, morin, and rutin), we observed that the affinities of these compounds for type‐II EBS are correlated with their growth‐inhibitory potential. Furthermore, the Q sensitivity of the colon cancer cell lines was correlated with the number of type‐II EBS/cell. Then Q could regulate colon cancer cell growth through a binding interaction with type‐ll EBS. This mechanism could also be active in vivo as we have observed that cytosolic type‐II EBS are present in primary colorectal cancers and that Q is effective in inhibiting the in vitro bromodeoxyuridine incorporated by neoplastic cells in these cancers.