Elucidation of molecular mechanisms of plasticity in tumor cells

2018 Fiscal Year Final Research Report

• Project/Area Number: 17K19587
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology and related fields
• Research Institution: Kanazawa University
• Principal Investigator: Gotoh Noriko 金沢大学, がん進展制御研究所, 教授 (10251448)
• Project Period (FY): 2017-06-30 – 2019-03-31
• Keywords: 乳癌 / 前癌状態 / 癌微小環境 / ErbB / 炎症

Outline of Final Research Achievements

Although it is known that inflammation is involved in the precancerous mammary tissues, the molecular mechanisms remain unknown. We have elucidated that FRS2beta, an adaptor for feedback inhibition of ErbB-ERK signaling, plays critical roles for evoking inflammation in the precancerous mammary tissues.
We further show that tumor cells without FRS2beta cannot grow fast due to lack of inflammation in the mammary tissues, however, they gradually adapt the condition and finally obtain ability to grow in the absence of inflammation. Epithelial-mesenchymal transdition mechanisms are involved.

Free Research Field

腫瘍生物学

Academic Significance and Societal Importance of the Research Achievements

FRS2betaは、超早期乳がんのバイオマーカーとなりえる（特許取得済み）。マンモグラフィーなどで精密検査となった症例に針生研が行われるが、このときにFRS2beta抗体で免疫染色を行うことにより、FRS2betaの発現が高ければがんの可能性が高くなる。私どもは、FRS2betaに対するモノクローナル抗体をすでに開発している。FRS2betaを標的とした予防策も期待できる。