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2015 Fiscal Year Final Research Report

Study of suppression of fibrosis and EMT in pancreatic cancer radiation therapy

Research Project

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Project/Area Number 25462107
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Digestive surgery
Research InstitutionKanazawa University

Principal Investigator

Nakagawara Hisatoshi  金沢大学, 大学病院, 助教 (30401904)

Co-Investigator(Kenkyū-buntansha) TAJIMA HIDEHIRO  金沢大学, 大学病院, 講師 (00436825)
Co-Investigator(Renkei-kenkyūsha) OHTA TETSUO  金沢大学, 医学系, 教授 (40194170)
Project Period (FY) 2013-04-01 – 2016-03-31
KeywordsEMT / 血小板凝集抑制 / HDAC阻害薬 / タキサン系抗がん剤
Outline of Final Research Achievements

We evaluated the effect of valproic acid (VPA) and taxan for radiosensitivity in esophageal cancer, and investigated inhibitory effect of Epithelial-mesenchymal transition (EMT) using VPA and taxan for pancreatic stellate. Correlation EMT and platelet aggregation in the microenvironment of pancreatic cancer was clarified. VPA enhances cancer cells radiosensitivity by chromatin decondensation and down regulation of DNA double strand break repair proteins. Docetaxel (DTX) induced G1 and G2-M accumulation in esophageal cancer cell, respectively. Low dose DTX could yield radiosensitivity with induction of G1 arrest, although low dose DTX had limited cytotoxic effect. It has been shown that taxan (paclitaxel) and histone deacetylase (HDAC) inhibitor (sodium valproate) suppress the induction of EMT in pancreatic stem cell line in current study. But it has also been shown that the suppression of platelet aggregation has an important role of inhibition of the EMT in pancreatic cancer.

Free Research Field

医歯薬学

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Published: 2017-05-10  

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