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2016 Fiscal Year Final Research Report

Molecular targeted medicine to inhibit cancer stemness

Research Project

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Project/Area Number 26293196
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionSaitama Medical University (2015-2016)
Niigata University (2014)

Principal Investigator

Kagamu Hiroshi  埼玉医科大学, 医学部, 教授 (30418686)

Co-Investigator(Kenkyū-buntansha) 矢野 聖二  金沢大学, がん進展制御研究所, 教授 (30294672)
梅津 哉  新潟大学, 医歯学総合病院, 准教授 (50251799)
土田 正則  新潟大学, 医歯学系, 教授 (60293221)
Project Period (FY) 2014-04-01 – 2017-03-31
KeywordsDDX3X / Wnt/β-catenin / VEGF
Outline of Final Research Achievements

EGFR-TKI has led to unprecedented results in lung cancer patients harboring activating EGFR mutations. However, the phenotypic diversity of cancer cells results in the survival of treatment-resistant cells. DDX3X is a RNA helicase and is involved in Wnt/β-catenin signal activation. We identified lung cancer cells that expressed DDX3X achieve cancer stem cell-like and mesenchymal properties resulting in EGFR-TKI resistance. Response rate of DDX3X positive EGFR mutant lung cancer patients was only 13.3 %. In this study, we demonstrated that Wnt/β-catenin or VEGFR signal inhibitors exhibited synergistic antitumor reactivity to break EGFR-TKI resistance. Clinical sample analyses revealed that DDX3X expression was accompanied withβ-catenin and VEGFR-2 expression. Our data indicate a novel mechanism how lung cancer cells harboring EGFR-activating mutations survive through EGFR-TKI treatment and have a clinical implication to develop a novel treatment for VEGFR- and β-catenin-signaling.

Free Research Field

呼吸器内科

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Published: 2018-03-22  

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