Function of Ppp6c as a tumor suppressor gene

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19081
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: Miyagi Prefectural Hospital Organization Miyagi Cancer Center
• Principal Investigator: HAYASHI Katuhisa 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (30726302)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 腫瘍

Outline of Final Research Achievements

Using a 2-stage skin carcinogenesis model, we found that a single DMBA application was sufficient to produce papillomas in Protein phosphatase 6 catalytic subunit (Ppp6c)-deficient skin. The data suggests that Ppp6c-deficient skin is predisposed to carcinogenesis initiated by DMBA. Ppp6c-deficient skin tissues show an enhanced inflammatory response following DMBA treatment. Ppp6c-deficient tissue samples exhibited thicker epidermis associated with hyperkeratosis, cellular infiltration of the dermis, and disappearance of subcutaneous fat tissue, indicating inflammatory and proliferative responses. Expression of inflammation-related genes is upregulated by DMBA treatment and that this effect that is more significant in Ppp6c-deficient skin. Molecular mechanism underlying its pathogenesis is thought to be that TNF-α- and IL-1β-dependent NF-kB signaling is enhanced in Ppp6c-deficient keratinocytes.

Free Research Field

医歯薬学