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Differential requirement for DNA methyltransferase 1 in maintaining human cancer cell gene promoter hypermethylation.

Previous work has shown that DNA hypermethylation of tumor suppressor genes in colorectal cancer cells may be maintained in the absence of the major mammalian methyltransferase, DNA methyltransferase 1 (DNMT1). In an effort to dissect the dependency on DNMT1 to maintain such hypermethylation in diff... Full description

Journal Title: Cancer research January 15, 2006, Vol.66(2), pp.729-735
Main Author: Ting, Angela H
Other Authors: Jair, Kam-Wing , Schuebel, Kornel E , Baylin, Stephen B
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0008-5472
Link: http://search.proquest.com/docview/70686079/?pq-origsite=primo
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title: Differential requirement for DNA methyltransferase 1 in maintaining human cancer cell gene promoter hypermethylation.
format: Article
creator:
  • Ting, Angela H
  • Jair, Kam-Wing
  • Schuebel, Kornel E
  • Baylin, Stephen B
subjects:
  • Breast Neoplasms–Genetics
  • Colorectal Neoplasms–Pathology
  • DNA (Cytosine-5-)-Methyltransferase 1–Genetics
  • DNA (Cytosine-5-)-Methyltransferases–Pathology
  • DNA Methylation–Metabolism
  • Female–Genetics
  • Gene Deletion–Pathology
  • Humans–Pathology
  • Promoter Regions, Genetic–Pathology
  • RNA, Small Interfering–Pathology
  • Transfection–Pathology
  • Tumor Cells, Cultured–Pathology
  • Urinary Bladder Neoplasms–Pathology
  • RNA, Small Interfering
  • DNA (Cytosine-5-)-Methyltransferase 1
  • DNA (Cytosine-5-)-Methyltransferases
  • Dnmt1 Protein, Human
ispartof: Cancer research, January 15, 2006, Vol.66(2), pp.729-735
description: Previous work has shown that DNA hypermethylation of tumor suppressor genes in colorectal cancer cells may be maintained in the absence of the major mammalian methyltransferase, DNA methyltransferase 1 (DNMT1). In an effort to dissect the dependency on DNMT1 to maintain such hypermethylation in different cancer types, we performed a systematic analysis of depletion of DNMT1 in colorectal (SW48), bladder (T24), and breast (T47D) cancer cells by DNMT1-specific small hairpin RNA (shRNA) targeting. We show that although DNMT1-deficient SW48 and T24 cells exhibited no observable growth defects and were able to maintain promoter hypermethylation, DNMT1-deficient T47D breast cells failed to form comparable numbers of colonies when stably selected for the incorporation of the DNMT1-specific shRNA expression vector, suggesting a growth defect with reduced levels of DNMT1. Further treatment of T47D cells with transient transfection of small interfering RNA targeting DNMT1 revealed that severely DNMT1-deficient T47D cells could not fully maintain promoter hypermethylation, and gene silencing was partially reversed at two of the three assayed loci. These observations suggest that human cancer cells may differ in their reliance on DNMT1 for maintaining DNA methylation.
language: eng
source:
identifier: ISSN: 0008-5472
fulltext: fulltext
issn:
  • 00085472
  • 0008-5472
url: Link


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titleDifferential requirement for DNA methyltransferase 1 in maintaining human cancer cell gene promoter hypermethylation.
creatorTing, Angela H ; Jair, Kam-Wing ; Schuebel, Kornel E ; Baylin, Stephen B
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ispartofCancer research, January 15, 2006, Vol.66(2), pp.729-735
identifierISSN: 0008-5472
subjectBreast Neoplasms–Genetics ; Colorectal Neoplasms–Pathology ; DNA (Cytosine-5-)-Methyltransferase 1–Genetics ; DNA (Cytosine-5-)-Methyltransferases–Pathology ; DNA Methylation–Metabolism ; Female–Genetics ; Gene Deletion–Pathology ; Humans–Pathology ; Promoter Regions, Genetic–Pathology ; RNA, Small Interfering–Pathology ; Transfection–Pathology ; Tumor Cells, Cultured–Pathology ; Urinary Bladder Neoplasms–Pathology ; RNA, Small Interfering ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; Dnmt1 Protein, Human
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descriptionPrevious work has shown that DNA hypermethylation of tumor suppressor genes in colorectal cancer cells may be maintained in the absence of the major mammalian methyltransferase, DNA methyltransferase 1 (DNMT1). In an effort to dissect the dependency on DNMT1 to maintain such hypermethylation in different cancer types, we performed a systematic analysis of depletion of DNMT1 in colorectal (SW48), bladder (T24), and breast (T47D) cancer cells by DNMT1-specific small hairpin RNA (shRNA) targeting. We show that although DNMT1-deficient SW48 and T24 cells exhibited no observable growth defects and were able to maintain promoter hypermethylation, DNMT1-deficient T47D breast cells failed to form comparable numbers of colonies when stably selected for the incorporation of the DNMT1-specific shRNA expression vector, suggesting a growth defect with reduced levels of DNMT1. Further treatment of T47D cells with transient transfection of small interfering RNA targeting DNMT1 revealed that severely DNMT1-deficient T47D cells could not fully maintain promoter hypermethylation, and gene silencing was partially reversed at two of the three assayed loci. These observations suggest that human cancer cells may differ in their reliance on DNMT1 for maintaining DNA methylation.
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