HPV-16 E6 and E7 oncogene expression is downregulated as a result of Mdm2 knockdown

被引：5
作者：
Diaz, Daniel [1 ]
Salinas Santander, Mauricio A. [2 ]
Morlett Chavez, Jesus A. [1 ]
机构：
[1] Univ Autonoma Coahuila, Dept Anal Clin & Diagnost Mol, Fac Chem, Saltillo 25280, Coahuila, Mexico
[2] Univ Autonoma Nuevo Leon, Dept Biochem & Mol Med, Fac Med, Monterrey, Nuevo Leon, Mexico
来源：
INTERNATIONAL JOURNAL OF ONCOLOGY | 2012年 / 41卷 / 01期
关键词：
cervical cancer; E6; E7; HPV-16; Mdm2; RNAi; HUMAN-PAPILLOMAVIRUS E6; CERVICAL-CARCINOMA CELLS; TUMOR-SUPPRESSOR; RNA INTERFERENCE; P53; MUTATIONS; CANCER CELLS; DEGRADATION; INHIBITION; PROTEIN; SIRNA;
D O I：
10.3892/ijo.2012.1429
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The carcinogenic potential of HPV infections is based on the integration and constitutive expression of the E6 and E7 genes which inhibit the p53 and Rb tumor suppressor proteins. In normal cells, Mdm2 regulates p53 in a negative feedback loop, and although Mdm2 is apparently functional in HPV-infected cells, E6 is the protein responsible for repressing p53 replacing Mdm2 function. The role of Mdm2 in HPV-positive cells is still elusive. In this study, Mdm2 was knocked down in an HPV-positive cervical cancer cell line; as a result we found downregulation of the expression of E6 and E7 and p53 upregulation.
引用
收藏
页码：141 / 146
页数：6
相关论文
共 36 条
  • [1] The epidemiology of human papillomavirus infections
    Baseman, JG
    Koutsky, LA
    [J]. JOURNAL OF CLINICAL VIROLOGY, 2005, 32 : S16 - S24
  • [2] PREVALENCE OF HUMAN PAPILLOMAVIRUS IN CERVICAL-CANCER - A WORLDWIDE PERSPECTIVE
    BOSCH, FX
    MANOS, MM
    MUNOZ, N
    SHERMAN, M
    JANSEN, AM
    PETO, J
    SCHIFFMAN, MH
    MORENO, V
    KURMAN, R
    SHAH, KV
    ALIHONOU, E
    BAYO, S
    MOKHTAR, HC
    CHICAREON, S
    DAUDT, A
    DELOSRIOS, E
    GHADIRIAN, P
    KITINYA, JN
    KOULIBALY, M
    NGELANGEL, C
    TINTORE, LMP
    RIOSDALENZ, JL
    SARJADI
    SCHNEIDER, A
    TAFUR, L
    TEYSSIE, AR
    ROLON, PA
    TORROELLA, M
    TAPIA, AV
    WABINGA, HR
    ZATONSKI, W
    SYLLA, B
    VIZCAINO, P
    MAGNIN, D
    KALDOR, J
    GREER, C
    WHEELER, C
    [J]. JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1995, 87 (11): : 796 - 802
  • [3] Boyer SN, 1996, CANCER RES, V56, P4620
  • [4] Induction of the p53-target gene GADD45 in HPV-positive cancer cells
    Butz, K
    Whitaker, N
    Denk, C
    Ullmann, A
    Geisen, C
    Hoppe-Seyler, F
    [J]. ONCOGENE, 1999, 18 (14) : 2381 - 2386
  • [5] Chen JD, 1996, MOL CELL BIOL, V16, P2445
  • [6] Human papillomavirus 16/18 E6 oncoprotein is expressed in lung cancer and related with p53 inactivation
    Cheng, Ya-Wen
    Wu, Nling-Fang
    Wang, John
    Yeh, Kun-Tu
    Goan, Yih-Gang
    Chiou, Hui-Ling
    Chen, Chih-Yi
    Lee, Huei
    [J]. CANCER RESEARCH, 2007, 67 (22) : 10686 - 10693
  • [7] TRANSIENT REPLICATION OF HUMAN PAPILLOMAVIRUS DNAS
    DELVECCHIO, AM
    ROMANCZUK, H
    HOWLEY, PM
    BAKER, CC
    [J]. JOURNAL OF VIROLOGY, 1992, 66 (10) : 5949 - 5958
  • [8] Different mechanisms contribute to the E2-mediated transcriptional repression of human papillomavirus type 18 viral oncogenes
    Demeret, C
    Desaintes, C
    Yaniv, M
    Thierry, F
    [J]. JOURNAL OF VIROLOGY, 1997, 71 (12) : 9343 - 9349
  • [9] p53 mutations are rare events in recurrent cervical cancer
    Denk, C
    Butz, K
    Schneider, A
    Dürst, M
    Hoppe-Seyler, F
    [J]. JOURNAL OF MOLECULAR MEDICINE-JMM, 2001, 79 (5-6): : 283 - 288
  • [10] THE MDM-2 ONCOGENE CAN OVERCOME WILD-TYPE P53 SUPPRESSION OF TRANSFORMED-CELL GROWTH
    FINLAY, CA
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (01) : 301 - 306
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