Application of self-organisation for cancer treatment

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K06891
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor therapeutics
• Research Institution: Japanese Foundation for Cancer Research
• Principal Investigator: Migita Toshiro 公益財団法人がん研究会, がん化学療法センター 分子生物治療研究部, 研究員 (20462236)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: がん幹細胞 / 自己組織化 / 分化

Outline of Final Research Achievements

c-myc is a driver oncogene of human liver cancer. We found that c-myc plays an important role in the maintenance of an undifferentiated state of liver cancer cell lines. c-myc depletion significantly inhibited the growth of liver cancer cells; however, it did not affect the level of alpha-fetoprotein (AFP), which is a marker of tumor malignancy.
ACTB, a gene encoding cytoskeletal beta-actin, is known as a target of cancer therapy. Inhibition of both c-myc and ACTB expression upregulated albumin expression, but downregulated AFP expression, suggesting the promotion of differentiation and the suppression of malignancy. Moreover, inhibition of both c-myc and ACTB expression strongly inhibited colony formation in 3D-culture compared to inhibition of c-myc alone, suggesting that inhibition of both c-myc and ACTB expression suppresses tumorigenicity.

Free Research Field

腫瘍学

Academic Significance and Societal Importance of the Research Achievements

細胞骨格遺伝子であるbeta-actinのがん細胞での役割については不明な点が多いが、正常細胞よりも量的に増加していることが多い。beta-actinとがん遺伝子であるc-mycを同時に抑制すると、分化促進と悪性度低下が見られたことより、がん細胞が機能的に正常化する可能性が示唆された。がん細胞特異的にbeta-actinの発現を抑制することができれば、beta-actinとc-mycの同時抑制は有望な治療法になると考えられた。