学术探索
学术期刊
新闻热点
数据分析
智能评审

OVEREXPRESSION OF HUMAN CYCLIN D1 REDUCES THE TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) TYPE-II RECEPTOR AND GROWTH-INHIBITION BY TGF-BETA-1 IN AN IMMORTALIZED HUMAN ESOPHAGEAL EPITHELIAL-CELL LINE

被引：88
作者：
OKAMOTO, A
JIANG, W
KIM, SJ
SPILLARE, EA
STONER, GD
WEINSTEIN, IB
HARRIS, CC
机构：
[1] NCI, HUMAN CARCINOGENESIS LAB, BETHESDA, MD 20892 USA
[2] NCI, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA
[3] OHIO STATE UNIV, COLUMBUS, OH 43210 USA
[4] COLUMBIA UNIV, COLUMBIA PRESBYTERIAN CANC CTR, NEW YORK, NY 10032 USA
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1994年 / 91卷 / 24期
关键词：
CARCINOGENESIS; G(1) CYCLIN; CELL CYCLE; CYCLIN DEPENDENT KINASE;
D O I：
10.1073/pnas.91.24.11576
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Cyclin D1 has been implicated in G(1) cell cycle progression and is frequently amplified, overtranscribed, and oversynthesized in human tumors, including esophageal carcinomas. To further address the role of cyclin D1 in cell cycle control and tumorigenesis, we have stably transfected the human cyclin D1 in the nontumorigenic esophageal epithelial cell line HET-1A. These transfected cells, which express increased amounts of cyclin D1, have enhanced colony-forming efficiency and saturation density and are resistant to growth inhibition by TGF-beta 1 compared with the parental cell line or a control vector cell clone. The clones which express increased amounts of cyclin D1 exhibited a decrease in the amount of TGF-beta type II receptor, indicating a plausible mechanism for their diminished response to TGF-beta 1. Therefore, deregulated expression of the cyclin D1 gene can modulate the negative growth factor pathway of TGF-beta 1 and may disturb the control of epithelial cell proliferation in esophageal carcinogenesis.
引用
收藏
页码：11576 / 11580
页数：5
相关论文
共 40 条
[1]   CYCLIN D1 IS A NUCLEAR-PROTEIN REQUIRED FOR CELL-CYCLE PROGRESSION IN G(1) [J].
BALDIN, V ;
LUKAS, J ;
MARCOTE, MJ ;
PAGANO, M ;
DRAETTA, G .
GENES & DEVELOPMENT, 1993, 7 (05) :812-821
[2]   A TRANSFORMING GROWTH-FACTOR-BETA TYPE-I RECEPTOR THAT SIGNALS TO ACTIVATE GENE-EXPRESSION [J].
BASSING, CH ;
YINGLING, JM ;
HOWE, DJ ;
WANG, TW ;
HE, WW ;
GUSTAFSON, ML ;
SHAH, P ;
DONAHOE, PK ;
WANG, XF .
SCIENCE, 1994, 263 (5143) :87-89
[3]  
BOYD FT, 1989, J BIOL CHEM, V264, P2272
[4]   WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].
ELDEIRY, WS ;
TOKINO, T ;
VELCULESCU, VE ;
LEVY, DB ;
PARSONS, R ;
TRENT, JM ;
LIN, D ;
MERCER, WE ;
KINZLER, KW ;
VOGELSTEIN, B .
CELL, 1993, 75 (04) :817-825
[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 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
[7]  
HARPER JW, 1993, CELL, V75, P805
[8]   FUNCTION OF A HUMAN CYCLIN GENE AS AN ONCOGENE [J].
HINDS, PW ;
DOWDY, SF ;
EATON, EN ;
ARNOLD, A ;
WEINBERG, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (02) :709-713
[9]   FREQUENT MUTATION OF THE P53 GENE IN HUMAN ESOPHAGEAL CANCER [J].
HOLLSTEIN, MC ;
METCALF, RA ;
WELSH, JA ;
MONTESANO, R ;
HARRIS, CC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (24) :9958-9961
[10]   GROWTH-INHIBITION BY TRANSFORMING GROWTH FACTOR-BETA(TGF-BETA) TYPE-I IS RESTORED IN TGF-BETA-RESISTANT HEPATOMA-CELLS AFTER EXPRESSION OF TGF-BETA RECEPTOR TYPE-II CDNA [J].
INAGAKI, M ;
MOUSTAKAS, A ;
LIN, HY ;
LODISH, HF ;
CARR, BI .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (11) :5359-5363
1234