HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma.

HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma. Research Abstract Details 

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HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma. Abstract Text:

Keishi Yamashita,Myoung Sook Kim,Hannah Lui Park,Yutaka Tokumaru,Motonobu Osada,Hiroshi Inoue,Masaki Mori,David Sidransky,Keishi Yamashita,Myoung Sook Kim,Hannah Lui Park,Yutaka Tokumaru,Motonobu Osada,Hiroshi Inoue,Masaki Mori,David Sidransky,

Promoter DNA hypermethylation with gene silencing is a common feature of human cancer, and cancer-prone methylation is believed to be a landmark of tumor suppressor genes (TSG). Identification of novel methylated genes would not only aid in the development of tumor markers but also elucidate the biological behavior of human cancers. We identified several epigenetically silenced candidate TSGs by pharmacologic unmasking of esophageal squamous cell carcinoma (ESCC) cell lines by demethylating agents (5-aza-2'-deoxycitidine and trichostatin A) combined with ESCC expression profiles using expression microarray. HOP/OB1/NECC1 was identified as an epigenetically silenced candidate TSG and further examined for (a) expression status, (b) methylation status, and (c) functional involvement in cancer cell lines. (a) The HOP gene encodes two putative promoters (promoters A and B) associated with two open reading frames (HOPalpha and HOPbeta, respectively), and HOPalpha and HOPbeta were both down-regulated in ESCC independently. (b) Promoter B harbors dense CpG islands, in which we found dense methylation in a cancer-prone manner (55% in tumor tissues by TaqMan methylation-specific PCR), whereas promoter A does not harbor CpG islands. HOPbeta silencing was associated with DNA methylation of promoter B in nine ESCC cell lines tested, and reactivated by optimal conditions of demethylating agents, whereas HOPalpha silencing was not reactivated by such treatments. Forced expression of HOP suppressed tumorigenesis in soft agar in four different squamous cell carcinoma cell lines. More convincingly, RNA interference knockdown of HOP in TE2 cells showed drastic restoration of the oncogenic phenotype. In conclusion, HOP is a putative TSG that harbors tumor inhibitory activity, and we for the first time showed that the final shutdown process of HOP expression is linked to promoter DNA hypermethylation under the double control of the discrete promoter regions in cancer. (Mol Cancer Res 2008;6(1):31-41).

HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma. Publishing Authors By Initials

K Yamashita,MS Kim,HL Park,Y Tokumaru,M Osada,H Inoue,M Mori,D Sidransky,K Yamashita,MS Kim,HL Park,Y Tokumaru,M Osada,H Inoue,M Mori,D Sidransky,

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HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Molecular cancer research : MCR

VOLUME: 6

Page Numbers: 31-41

Journal Abbreviation: Mol. Cancer Res.

ISSN: 1541-7786

DAY: 31

MONTH: Jan

YEAR: 2008

HOP/OB1/NECC1 Promoter DNA Is Frequently Hypermethylated and Involved in Tumorigenic Ability in Esophageal Squamous Cell Carcinoma. Information

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LANGUAGE: eng

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AFFILIATION: Department of Otolaryngology, Head and Neck Cancer Research Division, Johns Hopkins University, Baltimore, MD 21231. dsidrans@jhmi.edu.

Country: United States

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MEDLINETA: Mol Cancer Res

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