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Quercetin enhances transforming growth factor β 1 , secretion by human ovarian cancer cells
Author(s) -
Scambia Giovanni,
Panici Pierluigi Benedetti,
Ranelletti F. O.,
Ferrandina G.,
de Vincenzo R.,
Piantelli M.,
Masciullo V.,
Bonanno G.,
Isola G.,
Mancuso S.
Publication year - 1994
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.2910570214
Subject(s) - transforming growth factor beta , endocrinology , autocrine signalling , transforming growth factor , clonogenic assay , secretion , medicine , tgf beta signaling pathway , cell culture , beta (programming language) , biology , cell growth , receptor , growth factor , northern blot , cancer research , gene expression , biochemistry , gene , computer science , genetics , programming language
Our study demonstrates that quercetin (Q)‐induced growth‐inhibitory activity in ovarian cancer cells may be mediated by modulation of transforming growth factor β 1 (TGFβ 1 ) production. We used the OVCA 433 cell line which is very sensitive to the anti‐proliferative effect of Q and expresses high‐affinity, low‐capacity TGFβ 1 receptors. Conditioned medium (CM) from Q‐treated cells is able to displace 125I ‐TGFβ 1 from binding to its receptor; moreover Q (10 μM) increases TGFβ 1 activity in CM in a time‐dependent fashion starting after 4 hr and reaching a maximum by 24 hr of Q treatment. Q‐induced growth inhibition is reversed by a neutralizing anti‐TGFβ 1 MAb both in OVCA 433 and in a clonogenic assay of cells from a primary ovarian tumor. Q‐induced increase of TGFβ 1 activity in CM is specific since other anti‐proliferative compounds, such as Dexamethasone, which is as active on the cell cycle as Q, had no effect on TGFβ 1 secretion. Northorn‐blot analysis of TGFβ 1 mRNA levels at various times of Q (10 μM) exposure revealed that there was no increase, suggesting that regulation of TGFβ 1 occurs at post‐transcription at levels. © 1994 Wiley‐Liss, Inc.