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2015 Fiscal Year Final Research Report

Inflammatory circuit that triggres malignant progression

Research Project

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Project/Area Number 26640070
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Tumor biology
Research InstitutionKanazawa University

Principal Investigator

Takahashi Chiaki  金沢大学, がん進展制御研究所, 教授 (50283619)

Co-Investigator(Renkei-kenkyūsha) KITAJIMA Shunsuke  金沢大学, がん進展制御研究所, 教授 (90566465)
Project Period (FY) 2014-04-01 – 2016-03-31
Keywordsがん / 炎症 / RB / IL-6
Outline of Final Research Achievements

Retinoblastoma (RB) protein inactivation during tumor progression is often associated with a gain of immature phenotypes and chemo-resistance. Determination of an Rb inactivation signature in the context of gaining undifferentiated phenotype revealed that interleukin (IL)-6 is critically implicated in it. Breast cancers are often characterized by RB pathway inactivation. Low RB expression is linked to poorer prognosis and higher IL-6 expression in cases of breast cancer. IL-6 secreted from human breast cancers appeared to determine their tumor-initiating ability and chemo-resistance by promoting a positive feed forward loop between IL-6 and STAT3. The mechanism whereby RB inactivation increased IL-6 production involved fatty acid oxidation (FAO)-dependent mitochondrial metabolism. In addition, IL-6, via STAT3-mediated feedback to mitochondria, autonomously adjusts mitochondrial superoxide to levels suitable to maintain stem cell-like activity.

Free Research Field

腫瘍分子生物学

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Published: 2017-05-10  

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