Highly metastatic mouse mammary carcinoma cells decrease suppressive miRNAs via exosome

2019 Fiscal Year Final Research Report

• Project/Area Number: 16K10482
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General surgery
• Research Institution: Osaka Medical College
• Principal Investigator: ITO YUKO 大阪医科大学, その他部局等, 功労教授 (40148432)
• Co-Investigator(Kenkyū-buntansha): 柴田 雅朗 大阪医科大学, 医学部, 准教授 (10319543) ; Eid NabilA.S. 大阪医科大学, 医学部, 講師 (50570165) ; 濱岡 仁美 (黒瀬仁美) 大阪医科大学, 医学部, 講師 (80545608)
• Project Period (FY): 2016-04-01 – 2020-03-31
• Keywords: 乳がん / リンパ行性転移 / VEGF-C / Exosome / microRNA / hypoxia

Outline of Final Research Achievements

We previously reported that high expression level of VEGF-C in mouse mammary carcinoma cell (BJMC3879) caused high metastatic propensity to lymph nodes or lungs because of its ability for lymphangiogenesis. This study was aimed to demonstrate the role of the exosome mouse mammary carcinoma cell-derived, for metastasis. We hypothesized that excessive expression of miR-27b suppressed expression of VEGF-C in BJMC3879 cell was removed via secretion of exosome under the severe environment such a hypoxia condition, and BJMC3879 could proliferate by VEGF-C/VEGFR-3 system. BJMC3879 could use their exosomes containing VEGF-C due to VEGFR-3-expression on their cell membrane.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

miR-27bのexosomeによる排出を止める、またはmiR-27bを遺伝子導入すればVEGF-Cの発現が低下し、乳癌の増殖、転移をおさえることができる。女性の死亡原因の上位にある乳癌の核酸医学的治療の基礎をかためることができたと言える。