JARID2 is involved in transforming growth factor-beta-induced epithelial-mesenchymal transition of lung and colon cancer cell lines

Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involv...

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Published inPloS one Vol. 9; no. 12; p. e115684
Main Authors Tange, Shoichiro, Oktyabri, Dulamsuren, Terashima, Minoru, Ishimura, Akihiko, Suzuki, Takeshi
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 26.12.2014
Public Library of Science (PLoS)
Subjects
Biological activity
Biology and Life Sciences
Biotechnology
Bone morphogenetic proteins
Cadherins - genetics
Cadherins - metabolism
Cancer
Cell cycle
Chromatin
Colon
Colon cancer
Colonic Neoplasms - metabolism
Colorectal cancer
Development and progression
DNA methylation
E-cadherin
Enhancer of Zeste Homolog 2 Protein
Enzymes
Epigenetics
Epithelial-Mesenchymal Transition
Gene expression
Gene regulation
Gene silencing
Genes
Genomics
Growth factors
Histone H3
Histones - metabolism
HT29 Cells
Humans
Immunoprecipitation
Lung cancer
Lung diseases
Lung Neoplasms - metabolism
Lysine
Medical research
Medicine and Health Sciences
Mesenchyme
Methylation
MicroRNAs
MicroRNAs - genetics
miRNA
Polycomb group proteins
Polycomb Repressive Complex 2 - genetics
Polycomb Repressive Complex 2 - metabolism
Prostate
Proteins
Regulatory sequences
Ribonucleic acid
RNA
Stem cells
Studies
Transforming Growth Factor beta - pharmacology
Transforming growth factor-b
Transforming growth factors
Tumor cell lines
Online AccessGet full text

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Abstract Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in Transforming Growth Factor-beta (TGF-ß)-induced epithelial-mesenchymal transition (EMT) of A549 lung cancer cell line and HT29 colon cancer cell line. The expression of JARID2 was increased during TGF-ß-induced EMT of these cell lines and knockdown of JARID2 inhibited TGF-ß-induced morphological conversion of the cells associated with EMT. JARID2 knockdown itself had no effect in the expression of EMT-related genes but antagonized TGF-ß-dependent expression changes of EMT-related genes such as CDH1, ZEB family and microRNA-200 family. Chromatin immunoprecipitation assays showed that JARID2 was implicated in TGF-ß-induced transcriptional repression of CDH1 and microRNA-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of JARID2 protein, which may control PRC2 recruitment and histone methylation during TGF-ß-induced EMT of lung and colon cancer cell lines.
AbstractList Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in Transforming Growth Factor-beta (TGF-[beta])-induced epithelial-mesenchymal transition (EMT) of A549 lung cancer cell line and HT29 colon cancer cell line. The expression of JARID2 was increased during TGF-[beta]-induced EMT of these cell lines and knockdown of JARID2 inhibited TGF-[beta]-induced morphological conversion of the cells associated with EMT. JARID2 knockdown itself had no effect in the expression of EMT-related genes but antagonized TGF-[beta]-dependent expression changes of EMT-related genes such as CDH1, ZEB family and microRNA-200 family. Chromatin immunoprecipitation assays showed that JARID2 was implicated in TGF-[beta]-induced transcriptional repression of CDH1 and microRNA-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of JARID2 protein, which may control PRC2 recruitment and histone methylation during TGF-[beta]-induced EMT of lung and colon cancer cell lines.
Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in Transforming Growth Factor-beta (TGF-ß)-induced epithelial-mesenchymal transition (EMT) of A549 lung cancer cell line and HT29 colon cancer cell line. The expression of JARID2 was increased during TGF-ß-induced EMT of these cell lines and knockdown of JARID2 inhibited TGF-ß-induced morphological conversion of the cells associated with EMT. JARID2 knockdown itself had no effect in the expression of EMT-related genes but antagonized TGF-ß-dependent expression changes of EMT-related genes such as CDH1, ZEB family and microRNA-200 family. Chromatin immunoprecipitation assays showed that JARID2 was implicated in TGF-ß-induced transcriptional repression of CDH1 and microRNA-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of JARID2 protein, which may control PRC2 recruitment and histone methylation during TGF-ß-induced EMT of lung and colon cancer cell lines.
Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in Transforming Growth Factor-beta (TGF-ß)-induced epithelial-mesenchymal transition (EMT) of A549 lung cancer cell line and HT29 colon cancer cell line. The expression of JARID2 was increased during TGF-ß-induced EMT of these cell lines and knockdown of JARID2 inhibited TGF-ß-induced morphological conversion of the cells associated with EMT. JARID2 knockdown itself had no effect in the expression of EMT-related genes but antagonized TGF-ß-dependent expression changes of EMT-related genes such as CDH1 , ZEB family and microRNA-200 family. Chromatin immunoprecipitation assays showed that JARID2 was implicated in TGF-ß-induced transcriptional repression of CDH1 and microRNA-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of JARID2 protein, which may control PRC2 recruitment and histone methylation during TGF-ß-induced EMT of lung and colon cancer cell lines.
Audience Academic
Author Suzuki, Takeshi
Tange, Shoichiro
Ishimura, Akihiko
Terashima, Minoru
Oktyabri, Dulamsuren
AuthorAffiliation Seoul National University, Korea, Republic Of
Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan
AuthorAffiliation_xml – name: Seoul National University, Korea, Republic Of
– name: Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan
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  givenname: Dulamsuren
  surname: Oktyabri
  fullname: Oktyabri, Dulamsuren
  organization: Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan
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  givenname: Minoru
  surname: Terashima
  fullname: Terashima, Minoru
  organization: Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan
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  surname: Ishimura
  fullname: Ishimura, Akihiko
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  givenname: Takeshi
  surname: Suzuki
  fullname: Suzuki, Takeshi
  organization: Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25542019$$D View this record in MEDLINE/PubMed
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2014 Tange et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Competing Interests: The authors have declared that no competing interests exist.
Conceived and designed the experiments: ST DO TS. Performed the experiments: ST DO. Analyzed the data: MT AI. Wrote the paper: TS.
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Snippet Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that...
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StartPage e115684
SubjectTerms Biological activity
Biology and Life Sciences
Biotechnology
Bone morphogenetic proteins
Cadherins - genetics
Cadherins - metabolism
Cancer
Cell cycle
Chromatin
Colon
Colon cancer
Colonic Neoplasms - metabolism
Colorectal cancer
Development and progression
DNA methylation
E-cadherin
Enhancer of Zeste Homolog 2 Protein
Enzymes
Epigenetics
Epithelial-Mesenchymal Transition
Gene expression
Gene regulation
Gene silencing
Genes
Genomics
Growth factors
Histone H3
Histones - metabolism
HT29 Cells
Humans
Immunoprecipitation
Lung cancer
Lung diseases
Lung Neoplasms - metabolism
Lysine
Medical research
Medicine and Health Sciences
Mesenchyme
Methylation
MicroRNAs
MicroRNAs - genetics
miRNA
Polycomb group proteins
Polycomb Repressive Complex 2 - genetics
Polycomb Repressive Complex 2 - metabolism
Prostate
Proteins
Regulatory sequences
Ribonucleic acid
RNA
Stem cells
Studies
Transforming Growth Factor beta - pharmacology
Transforming growth factor-b
Transforming growth factors
Tumor cell lines
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Title JARID2 is involved in transforming growth factor-beta-induced epithelial-mesenchymal transition of lung and colon cancer cell lines
URI https://www.ncbi.nlm.nih.gov/pubmed/25542019
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https://pubmed.ncbi.nlm.nih.gov/PMC4277293
https://doaj.org/article/e1cdd92f0a184722a973b2f6b6a95ef5
http://dx.doi.org/10.1371/journal.pone.0115684
Volume 9
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