Identification of Semaphorin3B as a direct target of p53

Kensuke Ochi; Toshiki Mori; Yoshiaki Toyama; Yusuke Nakamura; Hirofumi Arakawa

doi:10.1038/sj/neo/7900211

Identification of Semaphorin3B as a direct target of p53

Kensuke Ochi, Toshiki Mori, Yoshiaki Toyama, Yusuke Nakamura, Hirofumi Arakawa

Research output: Contribution to journal › Article › peer-review

56 Citations (Scopus)

Abstract

A cDNA microarray analysis indicated that Semaphorin3B (Sema3B), a gene whose product is involved in axon guidance and axonal repulsion, is inducible by p53. Introduction of exogenous p53 into a glioblastoma cell line lacking wild-type p53 (U373MG) dramatically induced expression of Sema3B mRNA. An electrophoretic mobility shift assay and a reporter assay confirmed that a potential p53 binding site present in the promoter region had p53-dependent transcriptional activity. Expression of endogenous Sema3B was induced in response to genotoxic stresses caused by adriamycin treatment or UV irradiation in a p53-dependent manner. Ectopic expression of Sema3B in p53-defective cells reduced the number of colonies in colony formation assays. These results suggest that Sema3B might play some role in regulating cell growth as a mediator of p53 tumor-suppressor activity.

Original language	English
Pages (from-to)	82-87
Number of pages	6
Journal	Neoplasia
Volume	4
Issue number	1
DOIs	https://doi.org/10.1038/sj/neo/7900211
Publication status	Published - 2002
Externally published	Yes

Keywords

Apoptosis
Growth suppression
Semaphorin3B
Target gene
p53

ASJC Scopus subject areas

Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/sj/neo/7900211

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@article{dba09ecd1ee0464d9e1c5e1139736cbe,

title = "Identification of Semaphorin3B as a direct target of p53",

abstract = "A cDNA microarray analysis indicated that Semaphorin3B (Sema3B), a gene whose product is involved in axon guidance and axonal repulsion, is inducible by p53. Introduction of exogenous p53 into a glioblastoma cell line lacking wild-type p53 (U373MG) dramatically induced expression of Sema3B mRNA. An electrophoretic mobility shift assay and a reporter assay confirmed that a potential p53 binding site present in the promoter region had p53-dependent transcriptional activity. Expression of endogenous Sema3B was induced in response to genotoxic stresses caused by adriamycin treatment or UV irradiation in a p53-dependent manner. Ectopic expression of Sema3B in p53-defective cells reduced the number of colonies in colony formation assays. These results suggest that Sema3B might play some role in regulating cell growth as a mediator of p53 tumor-suppressor activity.",

keywords = "Apoptosis, Growth suppression, Semaphorin3B, Target gene, p53",

author = "Kensuke Ochi and Toshiki Mori and Yoshiaki Toyama and Yusuke Nakamura and Hirofumi Arakawa",

note = "Funding Information: Abbreviations: p53BS, p53 binding site; Sema3B, Semaphorin3B; Sema3A, Semaphorin3A; NRP1, neurophilin - 1; VEGF, vascular endothelial growth factor Address all correspondence to: Dr. Hirofumi Arakawa, Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6 -1 Shirokanedai, Minato -ku, Tokyo 108 - 8639, Japan. E -mail: harakawa@ims.u-tokyo.ac.jp 1This work was supported by Grant #13216031 from the Ministry of Education, Cullture, Sports, Science and Technology to H.A., and by {\textquoteleft}{\textquoteleft}Research for the Future{\textquoteright}{\textquoteright} Program Grant #00L01402 from the Japan Society for the Promotion of Science to Y.N. Received 27 August 2001; Accepted 11 October 2001.",

year = "2002",

doi = "10.1038/sj/neo/7900211",

language = "English",

volume = "4",

pages = "82--87",

journal = "Neoplasia",

issn = "1522-8002",

publisher = "Elsevier Inc.",

number = "1",

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TY - JOUR

T1 - Identification of Semaphorin3B as a direct target of p53

AU - Ochi, Kensuke

AU - Mori, Toshiki

AU - Toyama, Yoshiaki

AU - Nakamura, Yusuke

AU - Arakawa, Hirofumi

N1 - Funding Information: Abbreviations: p53BS, p53 binding site; Sema3B, Semaphorin3B; Sema3A, Semaphorin3A; NRP1, neurophilin - 1; VEGF, vascular endothelial growth factor Address all correspondence to: Dr. Hirofumi Arakawa, Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6 -1 Shirokanedai, Minato -ku, Tokyo 108 - 8639, Japan. E -mail: harakawa@ims.u-tokyo.ac.jp 1This work was supported by Grant #13216031 from the Ministry of Education, Cullture, Sports, Science and Technology to H.A., and by ‘‘Research for the Future’’ Program Grant #00L01402 from the Japan Society for the Promotion of Science to Y.N. Received 27 August 2001; Accepted 11 October 2001.

PY - 2002

Y1 - 2002

N2 - A cDNA microarray analysis indicated that Semaphorin3B (Sema3B), a gene whose product is involved in axon guidance and axonal repulsion, is inducible by p53. Introduction of exogenous p53 into a glioblastoma cell line lacking wild-type p53 (U373MG) dramatically induced expression of Sema3B mRNA. An electrophoretic mobility shift assay and a reporter assay confirmed that a potential p53 binding site present in the promoter region had p53-dependent transcriptional activity. Expression of endogenous Sema3B was induced in response to genotoxic stresses caused by adriamycin treatment or UV irradiation in a p53-dependent manner. Ectopic expression of Sema3B in p53-defective cells reduced the number of colonies in colony formation assays. These results suggest that Sema3B might play some role in regulating cell growth as a mediator of p53 tumor-suppressor activity.

AB - A cDNA microarray analysis indicated that Semaphorin3B (Sema3B), a gene whose product is involved in axon guidance and axonal repulsion, is inducible by p53. Introduction of exogenous p53 into a glioblastoma cell line lacking wild-type p53 (U373MG) dramatically induced expression of Sema3B mRNA. An electrophoretic mobility shift assay and a reporter assay confirmed that a potential p53 binding site present in the promoter region had p53-dependent transcriptional activity. Expression of endogenous Sema3B was induced in response to genotoxic stresses caused by adriamycin treatment or UV irradiation in a p53-dependent manner. Ectopic expression of Sema3B in p53-defective cells reduced the number of colonies in colony formation assays. These results suggest that Sema3B might play some role in regulating cell growth as a mediator of p53 tumor-suppressor activity.

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KW - Growth suppression

KW - Semaphorin3B

KW - Target gene

KW - p53

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Identification of Semaphorin3B as a direct target of p53

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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