Transcriptional control of the RECK metastasis/angiogenesis suppressor gene

Regina Maki Sasahara, Sheila Maria Brochado, Chiaki Takahashi, Jun Seo Oh, Silvya Stuchi Maria-Engler, José Mauro Granjeiro, Makoto Noda, Mari Cleide Sogayar

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

The RECK gene is widely expressed in normal human tissues but is downregulated in tumor cell lines and oncogenically transformed fibroblasts. RECK encodes a membrane-anchored glycoprotein that suppresses tumor invasion and angiogenesis by regulating matrix-metalloproteinases (MMP-2, MMP-9 and MT1-MMP). Understanding of the transcriptional regulation of tumor/metastasis suppressor genes constitutes a potent approach to the molecular basis of malignant transformation. In order to uncover the mechanisms of control of RECK gene expression, the RECK promoter has been cloned and characterized. One of the elements responsible for the Ras-mediated downregulation of mouse RECK gene is the Sp1 site, to which Sp1 and Sp3 factors bind. Other regulatory events, such as DNA methylation of the RECK promoter and histone acetylation/deacetylation have been studied to understand the underlying mechanisms of RECK expression. Understanding of the mechanisms which control RECK gene transcription may lead to the development of new strategies for cancer prevention and treatment.

Original languageEnglish
Pages (from-to)435-443
Number of pages9
JournalCancer Detection and Prevention
Volume26
Issue number6
DOIs
Publication statusPublished - 2002 Dec 1
Externally publishedYes

Fingerprint

Tumor Suppressor Genes
Matrix Metalloproteinases
Down-Regulation
Genes
Matrix Metalloproteinase 14
Matrix Metalloproteinase 2
Membrane Glycoproteins
DNA Methylation
Acetylation
Tumor Cell Line
Histones
Neoplasms
Fibroblasts
Gene Expression

Keywords

  • Angiogenesis
  • Metastasis
  • Sp1 transcription factor
  • Transcriptional control
  • Tumor suppressor gene

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Sasahara, R. M., Brochado, S. M., Takahashi, C., Oh, J. S., Maria-Engler, S. S., Granjeiro, J. M., ... Sogayar, M. C. (2002). Transcriptional control of the RECK metastasis/angiogenesis suppressor gene. Cancer Detection and Prevention, 26(6), 435-443. https://doi.org/10.1016/S0361-090X(02)00123-X

Transcriptional control of the RECK metastasis/angiogenesis suppressor gene. / Sasahara, Regina Maki; Brochado, Sheila Maria; Takahashi, Chiaki; Oh, Jun Seo; Maria-Engler, Silvya Stuchi; Granjeiro, José Mauro; Noda, Makoto; Sogayar, Mari Cleide.

In: Cancer Detection and Prevention, Vol. 26, No. 6, 01.12.2002, p. 435-443.

Research output: Contribution to journalArticle

Sasahara, RM, Brochado, SM, Takahashi, C, Oh, JS, Maria-Engler, SS, Granjeiro, JM, Noda, M & Sogayar, MC 2002, 'Transcriptional control of the RECK metastasis/angiogenesis suppressor gene', Cancer Detection and Prevention, vol. 26, no. 6, pp. 435-443. https://doi.org/10.1016/S0361-090X(02)00123-X
Sasahara RM, Brochado SM, Takahashi C, Oh JS, Maria-Engler SS, Granjeiro JM et al. Transcriptional control of the RECK metastasis/angiogenesis suppressor gene. Cancer Detection and Prevention. 2002 Dec 1;26(6):435-443. https://doi.org/10.1016/S0361-090X(02)00123-X
Sasahara, Regina Maki ; Brochado, Sheila Maria ; Takahashi, Chiaki ; Oh, Jun Seo ; Maria-Engler, Silvya Stuchi ; Granjeiro, José Mauro ; Noda, Makoto ; Sogayar, Mari Cleide. / Transcriptional control of the RECK metastasis/angiogenesis suppressor gene. In: Cancer Detection and Prevention. 2002 ; Vol. 26, No. 6. pp. 435-443.
@article{e6f90bfe85c64ab2aa40bb24d1ab5019,
title = "Transcriptional control of the RECK metastasis/angiogenesis suppressor gene",
abstract = "The RECK gene is widely expressed in normal human tissues but is downregulated in tumor cell lines and oncogenically transformed fibroblasts. RECK encodes a membrane-anchored glycoprotein that suppresses tumor invasion and angiogenesis by regulating matrix-metalloproteinases (MMP-2, MMP-9 and MT1-MMP). Understanding of the transcriptional regulation of tumor/metastasis suppressor genes constitutes a potent approach to the molecular basis of malignant transformation. In order to uncover the mechanisms of control of RECK gene expression, the RECK promoter has been cloned and characterized. One of the elements responsible for the Ras-mediated downregulation of mouse RECK gene is the Sp1 site, to which Sp1 and Sp3 factors bind. Other regulatory events, such as DNA methylation of the RECK promoter and histone acetylation/deacetylation have been studied to understand the underlying mechanisms of RECK expression. Understanding of the mechanisms which control RECK gene transcription may lead to the development of new strategies for cancer prevention and treatment.",
keywords = "Angiogenesis, Metastasis, Sp1 transcription factor, Transcriptional control, Tumor suppressor gene",
author = "Sasahara, {Regina Maki} and Brochado, {Sheila Maria} and Chiaki Takahashi and Oh, {Jun Seo} and Maria-Engler, {Silvya Stuchi} and Granjeiro, {Jos{\'e} Mauro} and Makoto Noda and Sogayar, {Mari Cleide}",
year = "2002",
month = "12",
day = "1",
doi = "10.1016/S0361-090X(02)00123-X",
language = "English",
volume = "26",
pages = "435--443",
journal = "Cancer Epidemiology",
issn = "1877-7821",
publisher = "Elsevier BV",
number = "6",

}

TY - JOUR

T1 - Transcriptional control of the RECK metastasis/angiogenesis suppressor gene

AU - Sasahara, Regina Maki

AU - Brochado, Sheila Maria

AU - Takahashi, Chiaki

AU - Oh, Jun Seo

AU - Maria-Engler, Silvya Stuchi

AU - Granjeiro, José Mauro

AU - Noda, Makoto

AU - Sogayar, Mari Cleide

PY - 2002/12/1

Y1 - 2002/12/1

N2 - The RECK gene is widely expressed in normal human tissues but is downregulated in tumor cell lines and oncogenically transformed fibroblasts. RECK encodes a membrane-anchored glycoprotein that suppresses tumor invasion and angiogenesis by regulating matrix-metalloproteinases (MMP-2, MMP-9 and MT1-MMP). Understanding of the transcriptional regulation of tumor/metastasis suppressor genes constitutes a potent approach to the molecular basis of malignant transformation. In order to uncover the mechanisms of control of RECK gene expression, the RECK promoter has been cloned and characterized. One of the elements responsible for the Ras-mediated downregulation of mouse RECK gene is the Sp1 site, to which Sp1 and Sp3 factors bind. Other regulatory events, such as DNA methylation of the RECK promoter and histone acetylation/deacetylation have been studied to understand the underlying mechanisms of RECK expression. Understanding of the mechanisms which control RECK gene transcription may lead to the development of new strategies for cancer prevention and treatment.

AB - The RECK gene is widely expressed in normal human tissues but is downregulated in tumor cell lines and oncogenically transformed fibroblasts. RECK encodes a membrane-anchored glycoprotein that suppresses tumor invasion and angiogenesis by regulating matrix-metalloproteinases (MMP-2, MMP-9 and MT1-MMP). Understanding of the transcriptional regulation of tumor/metastasis suppressor genes constitutes a potent approach to the molecular basis of malignant transformation. In order to uncover the mechanisms of control of RECK gene expression, the RECK promoter has been cloned and characterized. One of the elements responsible for the Ras-mediated downregulation of mouse RECK gene is the Sp1 site, to which Sp1 and Sp3 factors bind. Other regulatory events, such as DNA methylation of the RECK promoter and histone acetylation/deacetylation have been studied to understand the underlying mechanisms of RECK expression. Understanding of the mechanisms which control RECK gene transcription may lead to the development of new strategies for cancer prevention and treatment.

KW - Angiogenesis

KW - Metastasis

KW - Sp1 transcription factor

KW - Transcriptional control

KW - Tumor suppressor gene

UR - http://www.scopus.com/inward/record.url?scp=0036919274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036919274&partnerID=8YFLogxK

U2 - 10.1016/S0361-090X(02)00123-X

DO - 10.1016/S0361-090X(02)00123-X

M3 - Article

VL - 26

SP - 435

EP - 443

JO - Cancer Epidemiology

JF - Cancer Epidemiology

SN - 1877-7821

IS - 6

ER -