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Jumonji/Arid1b (Jarid1b) protein modulates human esophageal cancer cell growth
Author(s) -
Yoshihiro Kano,
Masamitsu Konno,
Katsuya Ohta,
Naotsugu Haraguchi,
Shimpei Nishikawa,
Yoshinori Kagawa,
Atsushi Hamabe,
Shinichiro Hasegawa,
Hisataka Ogawa,
Takahito Fukusumi,
Yuko Noguchi,
Miyuki Ozaki,
Toshihiro Kudo,
Daisuke Sakai,
Taroh Satoh,
Masaru Ishii,
Eiichi Mizohata,
Takeshi Inoue,
Masaki Mori,
Yuichiro� Doki,
Hideshi Ishii
Publication year - 2013
Publication title -
molecular and clinical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.442
H-Index - 7
eISSN - 2049-9469
pISSN - 2049-9450
DOI - 10.3892/mco.2013.127
Subject(s) - cancer research , biology , epigenetics , cancer , oncogene , esophageal cancer , cancer stem cell , cell growth , cell , cell cycle , stem cell , microbiology and biotechnology , biochemistry , genetics , gene
Although esophageal cancer is highly heterogeneous and the involvement of epigenetic regulation of cancer stem cells is highly suspected, the biological significance of epigenetically modified molecules that regulate different subpopulations remains to be firmly established. Using esophageal cancer cells, we investigated the functional roles of the H3K4 demethylase Jumonji/Arid1b (Jarid1b) (Kdm5b/Plu-1/Rbp2-h1), an epigenetic factor that is required for continuous cell growth in melanoma. JARID1B knockdown resulted in the suppression of esophageal cancer cell growth, sphere formation and invasion ability and was associated with loss of epithelial marker expression. However, these inhibitory effects observed on tumor formation were reverted subsequent to subcutaneous inoculation of these cells into immune-deficient mice. These results indicated that JARID1B plays a role in maintaining cancer stem cells in the esophagus and justifies the rationale for studying the effects of continuous inhibition of this epigenetic factor in esophageal cancer.

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