Functions of p63 exoressed in hepatocellular carcinoma: DNA damage responses and relation to virus-induced carcinogenesis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460475
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: University of Yamanashi
• Principal Investigator: KATOH Iyoko 山梨大学, 総合研究部, 准教授 (20333297)
• Co-Investigator(Renkei-kenkyūsha): MORIISHI Kohji 山梨大学, 総合研究部, 教授 (90260273) ; KURATA Shun-ichi 神奈川歯科大学, 歯学部, 特任教授 (60140901)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: p63

Outline of Final Research Achievements

This study investigated physical and functional interactions between p63, a member of the tumor suppressor p53 gene family, and hepatitis virus -related factors to detect the possible involvement of p63 in hepatocellular carcinogenesis. Interestingly, most of the hepatocellular carcinoma lines tested efficiently expressed the TA isoforms of p63 (TAp63) corresponding to p53. However, TAp63 did not respond to drug-induced DNA damage. No significant molecular interaction was evident between p63 and virus-related factors. Importantly, both HBV and HCV are known to activate the Wnt/beta-catenin signal transduction leading to carcinogenesis and malignancy. Our results showed interference of the Wnt-induced transcriptional activation by DeltaNp63alpha, indicating that hepatocellular carcinogenesis could be suppressed if the DeltaN isoform is expressed.

Free Research Field

分子腫瘍学