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Abnormal DNA methylation of CD133 in colorectal and glioblastoma tumors.

Much recent effort has focused on identifying and characterizing cellular markers that distinguish tumor propagating cells (TPC) from more differentiated progeny. We report here an unusual promoter DNA methylation pattern for one such marker, the cell surface antigen CD133 (Prominin 1). This protein... Full description

Journal Title: Cancer research October 1, 2008, Vol.68(19), pp.8094-8103
Main Author: Yi, Joo Mi
Other Authors: Tsai, Hsing-Chen , Glöckner, Sabine C , Lin, Steven , Ohm, Joyce E , Easwaran, Hari , James, C David , Costello, Joseph F , Riggins, Gregory , Eberhart, Charles G , Laterra, John , Vescovi, Angelo L , Ahuja, Nita , Herman, James G , Schuebel, Kornel E , Baylin, Stephen B
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-07-6208
Link: http://search.proquest.com/docview/69623593/?pq-origsite=primo
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title: Abnormal DNA methylation of CD133 in colorectal and glioblastoma tumors.
format: Article
creator:
  • Yi, Joo Mi
  • Tsai, Hsing-Chen
  • Glöckner, Sabine C
  • Lin, Steven
  • Ohm, Joyce E
  • Easwaran, Hari
  • James, C David
  • Costello, Joseph F
  • Riggins, Gregory
  • Eberhart, Charles G
  • Laterra, John
  • Vescovi, Angelo L
  • Ahuja, Nita
  • Herman, James G
  • Schuebel, Kornel E
  • Baylin, Stephen B
subjects:
  • Ac133 Antigen–Genetics
  • Animals–Metabolism
  • Antigens, CD–Therapeutic Use
  • Antineoplastic Agents–Analogs & Derivatives
  • Azacitidine–Therapeutic Use
  • Brain Neoplasms–Drug Therapy
  • Caco-2 Cells–Genetics
  • Carcinoma–Metabolism
  • Colorectal Neoplasms–Drug Therapy
  • DNA (Cytosine-5-)-Methyltransferases–Genetics
  • DNA Methylation–Metabolism
  • Decitabine–Drug Therapy
  • Female–Genetics
  • Gene Deletion–Metabolism
  • Gene Expression Regulation, Neoplastic–Antagonists & Inhibitors
  • Glioblastoma–Genetics
  • Glycoproteins–Drug Effects
  • Hct116 Cells–Drug Therapy
  • Ht29 Cells–Genetics
  • Humans–Metabolism
  • Mice–Genetics
  • Mice, Nude–Metabolism
  • Peptides–Genetics
  • Tumor Cells, Cultured–Metabolism
  • Xenograft Model Antitumor Assays–Metabolism
  • Ac133 Antigen
  • Antigens, CD
  • Antineoplastic Agents
  • Glycoproteins
  • Prom1 Protein, Human
  • Peptides
  • Prom1 Protein, Mouse
  • Decitabine
  • DNA (Cytosine-5-)-Methyltransferases
  • Azacitidine
ispartof: Cancer research, October 1, 2008, Vol.68(19), pp.8094-8103
description: Much recent effort has focused on identifying and characterizing cellular markers that distinguish tumor propagating cells (TPC) from more differentiated progeny. We report here an unusual promoter DNA methylation pattern for one such marker, the cell surface antigen CD133 (Prominin 1). This protein has been extensively used to enrich putative cancer propagating stem-like cell populations in epithelial tumors and, especially, glioblastomas. We find that, within individual cell lines of cultured colon cancers and glioblastomas, the promoter CpG island of CD133 is DNA methylated, primarily, in cells with absent or low expression of the marker protein, whereas lack of such methylation is evident in purely CD133+ cells. Differential histone modification marks of active versus repressed genes accompany these DNA methylation changes. This heterogeneous CpG island DNA methylation status in the tumors is unusual in that other DNA hypermethylated genes tested in such cultures preserve their methylation patterns between separated CD133+ and CD133- cell populations. Furthermore, the CD133 DNA methylation seems to constitute an abnormal promoter signature because it is not found in normal brain and colon but only in cultured and primary tumors. Thus, the DNA methylation is imposed on the transition between the active versus repressed transcription state for CD133 only in tumors. Our findings provide additional insight for the dynamics of aberrant DNA methylation associated with aberrant gene silencing in human tumors.
language: eng
source:
identifier: E-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-07-6208
fulltext: fulltext
issn:
  • 15387445
  • 1538-7445
url: Link


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titleAbnormal DNA methylation of CD133 in colorectal and glioblastoma tumors.
creatorYi, Joo Mi ; Tsai, Hsing-Chen ; Glöckner, Sabine C ; Lin, Steven ; Ohm, Joyce E ; Easwaran, Hari ; James, C David ; Costello, Joseph F ; Riggins, Gregory ; Eberhart, Charles G ; Laterra, John ; Vescovi, Angelo L ; Ahuja, Nita ; Herman, James G ; Schuebel, Kornel E ; Baylin, Stephen B
contributorYi, Joo Mi (correspondence author) ; Yi, Joo Mi (record owner)
ispartofCancer research, October 1, 2008, Vol.68(19), pp.8094-8103
identifierE-ISSN: 1538-7445 ; DOI: 10.1158/0008-5472.CAN-07-6208
subjectAc133 Antigen–Genetics ; Animals–Metabolism ; Antigens, CD–Therapeutic Use ; Antineoplastic Agents–Analogs & Derivatives ; Azacitidine–Therapeutic Use ; Brain Neoplasms–Drug Therapy ; Caco-2 Cells–Genetics ; Carcinoma–Metabolism ; Colorectal Neoplasms–Drug Therapy ; DNA (Cytosine-5-)-Methyltransferases–Genetics ; DNA Methylation–Metabolism ; Decitabine–Drug Therapy ; Female–Genetics ; Gene Deletion–Metabolism ; Gene Expression Regulation, Neoplastic–Antagonists & Inhibitors ; Glioblastoma–Genetics ; Glycoproteins–Drug Effects ; Hct116 Cells–Drug Therapy ; Ht29 Cells–Genetics ; Humans–Metabolism ; Mice–Genetics ; Mice, Nude–Metabolism ; Peptides–Genetics ; Tumor Cells, Cultured–Metabolism ; Xenograft Model Antitumor Assays–Metabolism ; Ac133 Antigen ; Antigens, CD ; Antineoplastic Agents ; Glycoproteins ; Prom1 Protein, Human ; Peptides ; Prom1 Protein, Mouse ; Decitabine ; DNA (Cytosine-5-)-Methyltransferases ; Azacitidine
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descriptionMuch recent effort has focused on identifying and characterizing cellular markers that distinguish tumor propagating cells (TPC) from more differentiated progeny. We report here an unusual promoter DNA methylation pattern for one such marker, the cell surface antigen CD133 (Prominin 1). This protein has been extensively used to enrich putative cancer propagating stem-like cell populations in epithelial tumors and, especially, glioblastomas. We find that, within individual cell lines of cultured colon cancers and glioblastomas, the promoter CpG island of CD133 is DNA methylated, primarily, in cells with absent or low expression of the marker protein, whereas lack of such methylation is evident in purely CD133+ cells. Differential histone modification marks of active versus repressed genes accompany these DNA methylation changes. This heterogeneous CpG island DNA methylation status in the tumors is unusual in that other DNA hypermethylated genes tested in such cultures preserve their methylation patterns between separated CD133+ and CD133- cell populations. Furthermore, the CD133 DNA methylation seems to constitute an abnormal promoter signature because it is not found in normal brain and colon but only in cultured and primary tumors. Thus, the DNA methylation is imposed on the transition between the active versus repressed transcription state for CD133 only in tumors. Our findings provide additional insight for the dynamics of aberrant DNA methylation associated with aberrant gene silencing in human tumors.
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titleAbnormal DNA methylation of CD133 in colorectal and glioblastoma tumors.
authorYi, Joo Mi ; Tsai, Hsing-Chen ; Glöckner, Sabine C ; Lin, Steven ; Ohm, Joyce E ; Easwaran, Hari ; James, C David ; Costello, Joseph F ; Riggins, Gregory ; Eberhart, Charles G ; Laterra, John ; Vescovi, Angelo L ; Ahuja, Nita ; Herman, James G ; Schuebel, Kornel E ; Baylin, Stephen B
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