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Expression and DNA methylation of SAMSN1 is associated with the malignant phenotype of hepatocellular carcinoma

Research Project

Project/Area Number 16K19890
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General surgery
Research InstitutionNagoya University

Principal Investigator

EZAKA Kazuhiro  名古屋大学, 医学部附属病院, 医員 (40772059)

Research Collaborator KANDA Mitsuro  名古屋大学, 医学部附属病院, 助教 (00644668)
Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords肝細胞癌 / DNAメチル化 / バイオマーカー / SAMSN1
Outline of Final Research Achievements

Identification of sensitive biomarkers for hepatocellular carcinoma (HCC) is required to achieve efficacious personalized therapy. We investigated its expression and methylation status of SAMSN1 in HCC. Analysis of HCC cell lines revealed that hypermethylation of the SAMSN1 promoter correlated with decreased expression of SAMSN1 mRNA and DNA demethylation increased SAMSN1 transcription. SAMSN1 was expressed at significantly lower levels in tumor tissue compared with the corresponding noncancerous tissues. Patients with extrahepatic recurrence exhibited the lowest levels of SAMSN1 expression in resected HCC tissues. The multivariate analysis identified SAMSN1 as an independent prognostic factor of HCC progression. The expression pattern of tissue SAMSN1 protein correlated with that of SAMSN1 mRNA. Circulating DNA methylation of SAMSN1 was difficult to be detected in serum samples. Our findings indicate that tissue SAMSN1 status represent a novel biomarker of the phenotype of HCC.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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