Identification of S100A2 as a target of the ΔNp63 oncogenic pathway

被引:0
作者
Hibi, K
Fujitake, S
Takase, T
Kodera, Y
Ito, K
Akiyama, S
Shirane, M
Nakao, A
机构
[1] Nagoya Univ, Grad Sch Med, Showa Ku, Nagoya, Aichi 4668560, Japan
[2] Nippon Roche Res Ctr, Dept Prod Res, Kanagawa 2478530, Japan
关键词
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose and Experimental Design: It has been proved recently that DeltaNp63 may play an oncogenic role in the tumorigenic pathway of squamous cell cancers. To gain additional insight into this pathway, we examined global patterns of gene expression in cancer cells after DeltaNp63 gene introduction using the oligonucleotide microarray approach. Results: We found that S100A2 might be a target of the DeltaNp63 pathway. To confirm the data obtained from oligonucleotide microarray, we then examined the interaction of DeltaNp63 to S100A2. S100A2 induction was strictly dependent on DeltaNp63 expression by DeltaNp63 transgene and Northern analysis. DeltaNp63 transactivated the S100A2 promoter, and significantly more fold changes were seen in DeltaNp63-introduced cells than in p53-introduced cells, suggesting that DeltaNp63 may be a novel stimulator of the S100A2 promoter. Conclusion: Taken together, this evidence would seem to suggest that S100A2 is a novel downstream mediator of DeltaNp63.
引用
收藏
页码:4282 / 4285
页数:4
相关论文
共 21 条
[1]   CHROMOSOME-17 DELETIONS AND P53 GENE-MUTATIONS IN COLORECTAL CARCINOMAS [J].
BAKER, SJ ;
FEARON, ER ;
NIGRO, JM ;
HAMILTON, SR ;
PREISINGER, AC ;
JESSUP, JM ;
VANTUINEN, P ;
LEDBETTER, DH ;
BARKER, DF ;
NAKAMURA, Y ;
WHITE, R ;
VOGELSTEIN, B .
SCIENCE, 1989, 244 (4901) :217-221
[2]  
Feng G, 2001, CANCER RES, V61, P7999
[3]   AIS is an oncogene amplified in squamous cell carcinoma [J].
Hibi, K ;
Trink, B ;
Patturajan, M ;
Westra, WH ;
Caballero, OL ;
Hill, DE ;
Ratovitski, EA ;
Jen, J ;
Sidransky, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (10) :5462-5467
[4]  
Hibi K, 1996, CANCER RES, V56, P480
[5]  
Hibi K, 2001, CLIN CANCER RES, V7, P469
[6]   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
[7]   DOWN-REGULATION OF A MEMBER OF THE S100 GENE FAMILY IN MAMMARY-CARCINOMA CELLS AND REEXPRESSION BY AZADEOXYCYTIDINE TREATMENT [J].
LEE, SW ;
TOMASETTO, C ;
SWISSHELM, K ;
KEYOMARSI, K ;
SAGER, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (06) :2504-2508
[8]  
Nylander K, 2000, INT J CANCER, V87, P368, DOI 10.1002/1097-0215(20000801)87:3<368::AID-IJC9>3.0.CO
[9]  
2-J
[10]   Cloning and functional analysis of human p51, which structurally and functionally resembles p53 [J].
Osada, M ;
Ohba, M ;
Kawahara, C ;
Ishioka, C ;
Kanamaru, R ;
Katoh, I ;
Ikawa, Y ;
Nimura, Y ;
Nakagawara, A ;
Obinata, M ;
Ikawa, S .
NATURE MEDICINE, 1998, 4 (07) :839-843