Elucidation of the role of Interleukin-32 involved in the invasive process of pancreatic cancer and its expression mechanism.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08707
• 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 Toyama
• Principal Investigator: Imura Johji 富山大学, 大学院医学薬学研究部(医学), 教授 (80316554)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 膵癌 / 浸潤 / IL-32

Outline of Final Research Achievements

This study was performed to investigate the invasiveness regulating factors that defines poor prognosis for pancreatic cancer. First, a highly invasive cell was established from the human-derived pancreatic cancer cell lines. IL-32 has been highly enhanced among several genes to expression. Furthermore it was confirmed whether IL-32 was involved in invasiveness. It was found that the invasiveness was inhibited by siRNA for IL-32, and the invasiveness was obtained when IL-32 was forcibly expressed in non-invasive cell. In pancreatic cancer tissues, the expression of IL-32 was not appeared in normal pancreatic ducts, was expressed in tumor cells, and it was particularly enhanced in the infiltrating area. The factors regulated by IL-32 were involved E-Cadherin, MMP4・14・9, Thrombospondin 1, Slug, BMP4 and etc.
From the above, it was suggested that IL-32 may be an important factor involved not only in inflammation but also in the invasiveness of pancreatic cancer.

Free Research Field

病理学

Academic Significance and Societal Importance of the Research Achievements

膵癌は最近、死亡率が増加の一途を辿っている。何故に、膵癌が予後不良なのか？その原因は数々あるが、特に膵癌は容易に周辺臓器に浸潤し易く、手術不能となることも要因である。では、なぜに易浸潤性なのか？浸潤を制御している機構や分子はどの様なものがあるのか？それらを明らかにすることが本研究の目的である。まず、浸潤性の高い細胞を作成し、これらで高発現している分子の中からL-32を見出した。さらに、IL-32を減少させると浸潤性が減弱し、亢進させると浸潤性を増すことを確認した。また、IL-32によって制御を受ける分子も明らかにした。今後、IL-32と共に、他の分子を抑制するような創薬にも繋がる研究である。