ANDROGENS INCREASE INSULIN-RECEPTOR MESSENGER-RNA LEVELS, INSULIN BINDING, AND INSULIN RESPONSIVENESS IN HEP-2 LARYNX-CARCINOMA CELLS

被引:19
作者
SESTI, G
MARINI, MA
BRIATA, P
TULLIO, AN
MONTEMURRO, A
BORBONI, P
DEPIRRO, R
GHERZI, R
LAURO, R
机构
[1] IST SCI STUDIO & CURA TUMORI,IST NAZL RIC CANC,CELLIFE LAB,VIALE BENEDETTO XV 10,I-16132 GENOA,ITALY
[2] IST SCI STUDIO & CURA TUMORI,IST NAZL RIC CANC,IMMUNOBIOL LAB,GENOA,ITALY
[3] UNIV ANCONA,CATTEDRA ENDOCRINOL,I-60100 ANCONA,ITALY
[4] UNIV ROME 2,DIPARTIMENTO MED INTERNA,CATTEDRA ENDOCRINOL 2,ROME,ITALY
关键词
INSULIN ACTION; INSULIN RECEPTOR GENE; ANDROGEN; HEP-2 LARYNX CARCINOMA;
D O I
10.1016/0303-7207(92)90181-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Androgen receptors have been found in human larynx and androgens have been supposed to play an important role in promoting the growth of laryngeal carcinomas. The molecular mechanism underlaying this phenomenon is not at all understood. Aim of this work was to investigate the effects of two androgens (testosterone and dihydrotestosterone) on insulin receptor mRNA levels and insulin binding activity as well as on either metabolic or growth-promoting actions of insulin in a human larynx carcinoma cell line (HEp-2). We found that HEp-2 cells express a high affinity insulin receptor. Both androgens significantly increase insulin receptor mRNA levels and insulin receptor number in HEp-2 cells. Insulin action, evaluated either as total glucose utilization or as [H-3]thymidine incorporation into DNA, significantly increased in HEp-2 treated with androgens in comparison to control cultures. Altogether, our data allow us to speculate that thc increased insulin effectiveness we observed in the larynx carcinoma cell line HEp-2 after androgen treatment might be involved in the regulation of larynx cancer cells growth.
引用
收藏
页码:111 / 118
页数:8
相关论文
共 37 条
[1]  
ARAKI E, 1987, J BIOL CHEM, V262, P16186
[2]   GENE-REGULATION BY STEROID-HORMONES [J].
BEATO, M .
CELL, 1989, 56 (03) :335-344
[3]   ANDROGEN STIMULATION AND LARYNGEAL DEVELOPMENT [J].
BECKFORD, NS ;
SCHAID, D ;
ROOD, SR ;
SCHANBACHER, B .
ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY, 1985, 94 (06) :634-640
[4]   CLONING AND CHARACTERIZATION OF A CDNA-ENCODING THE RAT-BRAIN GLUCOSE-TRANSPORTER PROTEIN [J].
BIRNBAUM, MJ ;
HASPEL, HC ;
ROSEN, OM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (16) :5784-5788
[5]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[6]   MULTIFACTORIAL CONTROL OF INSULIN-RECEPTOR GENE-EXPRESSION IN HUMAN CELL-LINES [J].
BRIATA, P ;
GHERZI, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 170 (03) :1184-1190
[7]   GLUCOSE STARVATION AND GLYCOSYLATION INHIBITORS REDUCE INSULIN-RECEPTOR GENE-EXPRESSION - CHARACTERIZATION AND POTENTIAL MECHANISM IN HUMAN-CELLS [J].
BRIATA, P ;
BRIATA, L ;
GHERZI, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 169 (02) :397-405
[8]   ISOLATION OF BIOLOGICALLY-ACTIVE RIBONUCLEIC-ACID FROM SOURCES ENRICHED IN RIBONUCLEASE [J].
CHIRGWIN, JM ;
PRZYBYLA, AE ;
MACDONALD, RJ ;
RUTTER, WJ .
BIOCHEMISTRY, 1979, 18 (24) :5294-5299
[9]  
CHOU CK, 1987, J BIOL CHEM, V262, P1842
[10]   INSULIN-STIMULATED GLUCOSE-TRANSPORT IN HUMAN ADIPOCYTES [J].
CIARALDI, TP ;
KOLTERMAN, OG ;
SIEGEL, JA ;
OLEFSKY, JM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1979, 236 (06) :E621-E625