RETRACTED: Endogenous control of cell cycle progression by autocrine transforming growth factor β in breast cancer cells (Retracted article. See vol. 79, pg. 1016, 2019)

被引:10
作者
Ammanamanchi, S
Tillekeratne, MPM
Ko, TC
Brattain, MG
机构
[1] Roswell Pk Canc Inst, Dept Pharmacol & Therapeut, Buffalo, NY 14263 USA
[2] Med Coll Ohio, Dept Pharmacol, Toledo, OH 43699 USA
[3] Univ Texas, Med Branch, Dept Surg, Galveston, TX 77550 USA
关键词
D O I
10.1158/0008-5472.CAN-03-2654
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tumor progression due to loss of autocrine negative transforming growth factor-beta (TGF-beta) activity was reported in various cancers of epithelial origin. Estrogen receptor expressing (ER+) breast cancer cells are refractory to TGF-beta effects and exhibit malignant behavior due to loss or inadequate expression of TGF-beta receptor type II (RII). The exogenous TGF-beta effects on the modulation of cell cycle machinery were analyzed previously. However, very little is known regarding the endogenous control of cell cycle progression by autocrine TGF-beta. In this study, we have used a tetracycline regulatable RII cDNA expression vector to demonstrate that RII replacement reconstitutes autocrine negative TGF-beta activity in ER+ breast cancer cells as evidenced by the delayed entry into S phase by the RII transfectants. Reversal of the delayed entry into S phase by the RII transfectants in the presence of tetracycline in addition to the decreased steady state transcription from a promoter containing the TGF-beta responsive element (p3TP-Lux) by TGF-beta neutralizing antibody treatment of the RII transfected cells confirmed that autocrine-negative TGF-beta activity was induced in the transfectants. Histone HI kinase assays indicated that the delayed entry of RII transfectants into phase was associated with markedly reduced cyclin-dependent kinase (CDK)2 kinase activity. This reduction in kinase activity was due to the induction of CDK inhibitors p21/waf1/cip1 and p27/kip, and their association with CDK2. Tetracycline treatment of RII transfectants led to the suppression of p21/waf1/cip1and p27/kip expression, thus, directly demonstrating induction of CDK inhibitors by autocrine TGF-beta leading to growth control of ER+ breast cancer cells.
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收藏
页码:2509 / 2515
页数:7
相关论文
共 30 条
[1]   Restoration of transforming growth factor-β signaling enhances radiosensitivity by altering the Bcl-2/Bax ratio in the p53 mutant pancreatic cancer cell line MIA PaCa-2 [J].
Ahmed, MM ;
Alcock, A ;
Chendil, D ;
Dey, S ;
Das, A ;
Venkatasubbarao, K ;
Mohiuddin, M ;
Sun, LZ ;
Strodel, WE ;
Freeman, JW .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (03) :2234-2246
[2]   Induction of transforming growth factor-β receptor type II expression in estrogen receptor-positive breast cancer cells through SP1 activation by 5-aza-2′-deoxycytidine [J].
Ammanamanchi, S ;
Kim, SJ ;
Sun, LZ ;
Brattain, MG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (26) :16527-16534
[3]   BOTH P16 AND P21 FAMILIES OF CYCLIN-DEPENDENT KINASE (CDK) INHIBITORS BLOCK THE PHOSPHORYLATION OF CYCLIN-DEPENDENT KINASES BY THE CDK-ACTIVATING KINASE [J].
APRELIKOVA, O ;
XIONG, Y ;
LIU, ET .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (31) :18195-18197
[4]   TRANSFORMING GROWTH-FACTOR-BETA INDUCES THE CYCLIN-DEPENDENT KINASE INHIBITOR P21 THROUGH A P53-INDEPENDENT MECHANISM [J].
DATTO, MB ;
LI, Y ;
PANUS, JF ;
HOWE, DJ ;
XIONG, Y ;
WANG, XF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (12) :5545-5549
[5]   TGF-BETA INHIBITION OF CDK4 SYNTHESIS IS LINKED TO CELL-CYCLE ARREST [J].
EWEN, ME ;
SLUSS, HK ;
WHITEHOUSE, LL ;
LIVINGSTON, DM .
CELL, 1993, 74 (06) :1009-1020
[6]   TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA)-INDUCED DOWN-REGULATION OF CYCLIN-A EXPRESSION REQUIRES A FUNCTIONAL TGF-BETA RECEPTOR COMPLEX - CHARACTERIZATION OF CHIMERIC AND TRUNCATED TYPE-I AND TYPE-II RECEPTORS [J].
FENG, XH ;
FILVAROFF, EH ;
DERYNCK, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (41) :24237-24245
[7]   TRANSFORMING GROWTH-FACTOR-BETA EFFECTS ON EXPRESSION OF G(1) CYCLINS AND CYCLIN-DEPENDENT PROTEIN-KINASES [J].
GENG, Y ;
WEINBERG, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (21) :10315-10319
[8]  
Gong JG, 2003, CANCER RES, V63, P3340
[9]   The MEK pathway is required for stimulation of p21WAF1/CIP1 by transforming growth factor-β [J].
Hu, PPC ;
Shen, X ;
Huang, D ;
Liu, YY ;
Counter, C ;
Wang, XF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (50) :35381-35387
[10]   Transcriptional repression of the transforming growth factor-β type I receptor gene by DNA methylation results in the development of TGF-β resistance in human gastric cancer [J].
Kang, SH ;
Bang, YJ ;
Im, YH ;
Yang, HK ;
Lee, DA ;
Lee, HY ;
Lee, HS ;
Kim, NK ;
Kim, SJ .
ONCOGENE, 1999, 18 (51) :7280-7286