Analysis of the mechanism of cancer progression that overcome the cellular senescence by activated Ras

2014 Fiscal Year Final Research Report

• Project/Area Number: 24501327
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: 防衛大学校(総合教育学群、人文社会科学群、応用科学群、電気情報学群及びシステム工学群) (2013-2014); National Center of Neurology and Psychiatry (2012)
• Principal Investigator: UEKITA TAKAMASA 防衛大学校(総合教育学群、人文社会科学群、応用科学群、電気情報学群及びシステム工, その他部局等, 准教授 (50373402)
• Co-Investigator(Renkei-kenkyūsha): YAMAGUCHI Hideki 国立がん研究センター, 難治進行がん研究分野, ユニット長 (10345035)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: Ras / CDCP1 / MMP / Invasion / Metastasis / ERK / Autophagy

Outline of Final Research Achievements

In normal cells, the expression of activated Ras induces cell death by cellular senescense, but recent evidence indicates a role in cancer progression, including metastasis and invasion; however, the mechanism is still unknown.
In this study, we present in vitro evidence that CDCP1 might play an essential role in supressing autophagy and cancer cell death by cellular scenesense. Activated Ras induces CDCP1 expression through authentic Ras-ERK signaling pathway.　Moreover, we found that CDCP1 induced by activated Ras controls cancer cell invasion through regulation of MMPs, such as MT1-MMP, MMP-2 and MMP-9.
These results indicate that CDCP1 is an essencial regulator of the cancer progression that overcome cell senescense.

Free Research Field

腫瘍生物学