In:
International Journal of Cancer, Wiley, Vol. 50, No. 3 ( 1992-02), p. 486-492
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.
Type of Medium:
Online Resource
ISSN:
0020-7136
,
1097-0215
DOI:
10.1002/ijc.2910500326
Language:
English
Publisher:
Wiley
Publication Date:
1992
detail.hit.zdb_id:
218257-9
detail.hit.zdb_id:
1474822-8
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