Growth Inhibition After Exposure to Transforming Growth Factor-beta1 in Human Bladder Cancer Cell Lines.
10.4111/kju.2014.55.7.487
- Author:
Changho LEE
1
;
Sang Han LEE
;
Doo Sang KIM
;
Yun Soo JEON
;
Nam Kyu LEE
;
Sang Eun LEE
Author Information
1. Department of Urology, Soonchunhyang University Cheonan Hospital, Cheonan, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Cell line;
Cell survival;
Transforming growth factor beta;
Urinary bladder neoplasms
- MeSH:
Antineoplastic Agents/administration & dosage/*pharmacology;
Apoptosis/drug effects;
Cell Line, Tumor/drug effects/pathology;
Cell Proliferation/drug effects;
Cell Separation/methods;
Dose-Response Relationship, Drug;
Drug Screening Assays, Antitumor/methods;
Flow Cytometry/methods;
Humans;
Transforming Growth Factor beta1/administration & dosage/*pharmacology;
Urinary Bladder Neoplasms/*pathology
- From:Korean Journal of Urology
2014;55(7):487-492
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Transforming growth factor-beta1 (TGF-beta1) plays a dual role in apoptosis and in proapoptotic responses in the support of survival in a variety of cells. The aim of this study was to determine the function of TGF-beta1 in bladder cancer cells. MATERIALS AND METHODS: The role of TGF-beta1 in bladder cancer cells was examined by observing cell viability by using the tetrazolium dye (MTT) assay after treating the bladder cancer cell lines 253J, 5637, T24, J82, HT1197, and HT1376 with TGF-beta1. Among these cell lines, the 253J and T24 cell lines were coincubated with TGF-beta1 and the pan anti-TGF-beta antibody. Fluorescence-activated cell sorter (FACS) analysis was performed to determine the mechanism involved after TGF-beta1 treatment in 253J cells. RESULTS: All six cell lines showed inhibited cellular growth after TGF-beta1 treatment. Although the T24 and J82 cell lines also showed inhibited cellular growth, the growth inhibition was less than that observed in the other 4 cell lines. The addition of pan anti-TGF-beta antibodies to the culture media restored the growth properties that had been inhibited by TGF-beta1. FACS analysis was performed in the 253J cells and the 253J cells with TGF-beta1. There were no significant differences in the cell cycle between the two treatments. However, there were more apoptotic cells in the TGF-beta1-treated 253J cells. CONCLUSIONS: TGF-beta1 did not stimulate cellular proliferation but was a growth inhibitory factor in bladder cancer cells. However, the pattern of its effects depended on the cell line. TGF-beta1 achieved growth inhibition by enhancing the level of apoptosis.
