Myc oncogene: a key component in cell cycle regulation and its implication for lung cancer

被引:95
作者
Zajac-Kaye, M [1 ]
机构
[1] Naval Hosp, Ctr Canc Res, NCI, NIH,Navy Oncol Branch, Bethesda, MD 20889 USA
关键词
Myc; lung cancer; cell cycle; pRB pathway; cyclins; cdk; cdk1;
D O I
10.1016/S0169-5002(01)00343-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The Myc gene family which includes c-Myc, N-Myc and L-Myc, are transcription factors that play a role in cell proliferation, apoptosis and in the development of human tumors. Myc amplification and overexpression has been detected in lung cancer of different histologic subtypes. Although the mechanism of Myc action is not yet fully understood, Myc has been proposed to play a role in growth control and cell cycle progression by stimulating and repressing the expression of key cell cycle regulators. This review will focus on the role of Myc in stimulating the G1/S transition of the cell cycle by regulating the levels and activity of cyclins, cyclin dependent kinases (cdk), cdk inhibitors and the pRb-binding transcription factor E2F. It is proposed that both the overexpression of Myc and the deregulation of the pRB/E2F pathway promotes the G1 to S transition in parallel by activating cyclinE/cdk2 complexes in lung cancer cells. Published by Elsevier Science Ireland Ltd.
引用
收藏
页码:S43 / S46
页数:4
相关论文
共 33 条
[1]  
ALEXANDROVA N, 1995, MOL CELL BIOL, V15, P5188
[2]   Induction of cyclin E-cdk2 kinase activity, E2F-dependent transcription and cell growth by Myc are genetically separable events [J].
Beier, R ;
Bürgin, A ;
Kiermaier, A ;
Fero, M ;
Karsunky, H ;
Saffrich, R ;
Möröy, T ;
Ansorge, W ;
Roberts, J ;
Eilers, M .
EMBO JOURNAL, 2000, 19 (21) :5813-5823
[3]   Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27 [J].
Bouchard, C ;
Thieke, K ;
Maier, A ;
Saffrich, R ;
Hanley-Hyde, J ;
Ansorge, W ;
Reed, S ;
Sicinski, P ;
Bartek, J ;
Eilers, M .
EMBO JOURNAL, 1999, 18 (19) :5321-5333
[4]  
BRENNAN J, 1991, CANCER RES, V51, P1708
[5]   EXPRESSION OF C-MYC IN PROGENITOR CELLS OF THE BRONCHOPULMONARY EPITHELIUM AND IN A LARGE NUMBER OF NONSMALL CELL LUNG CANCERS [J].
BROERS, JLV ;
VIALLET, J ;
JENSEN, SM ;
PASS, H ;
TRAVIS, WD ;
MINNA, JD ;
LINNOILA, RI .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1993, 9 (01) :33-43
[6]   Expression analysis with oligonucleotide microarrays reveals that MYC regulates genes involved in growth, cell cycle, signaling, and adhesion [J].
Coller, HA ;
Grandori, C ;
Tamayo, P ;
Colbert, T ;
Lander, ES ;
Eisenman, RN ;
Golub, TR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (07) :3260-3265
[7]   Development of pulmonary bronchiolo-alveolar adenocarcinomas in transgenic mice overexpressing murine c-myc and epidermal growth factor in alveolar type II pneumocytes [J].
Ehrhardt, A ;
Bartels, T ;
Geick, A ;
Klocke, R ;
Paul, D ;
Halter, R .
BRITISH JOURNAL OF CANCER, 2001, 84 (06) :813-818
[8]   The Myc/Max/Mad network and the transcriptional control of cell behavior [J].
Grandori, C ;
Cowley, SM ;
James, LP ;
Eisenman, RN .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 2000, 16 :653-699
[9]   BINDING AND SUPPRESSION OF THE MYC TRANSCRIPTIONAL ACTIVATION DOMAIN BY P107 [J].
GU, W ;
BHATIA, K ;
MAGRATH, IT ;
DANG, CV ;
DALLAFAVERA, R .
SCIENCE, 1994, 264 (5156) :251-254
[10]   Identification of CDK4 as a target of c-MYC [J].
Hermeking, H ;
Rago, C ;
Schuhmacher, M ;
Li, Q ;
Barrett, JF ;
Obaya, AJ ;
O'Connell, BC ;
Mateyak, MK ;
Tam, W ;
Kohlhuber, F ;
Dang, CV ;
Sedivy, JM ;
Eick, D ;
Vogelstein, B ;
Kinzler, KW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (05) :2229-2234