Personalized therapy targeting Met gene in lung cancer

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K09606
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Kanazawa University
• Principal Investigator: Kasahara Kazuo 金沢大学, 医学系, 准教授 (30272967)
• Co-Investigator(Kenkyū-buntansha): 曽根 崇 金沢大学, 医薬保健学総合研究科, 特任准教授 (30420334) ; 木村 英晴 金沢大学, 附属病院, 講師 (40444202)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: ｃMet / 非小細胞肺癌 / 個別化療法

Outline of Final Research Achievements

We examined cMet expression and phosphorylation in non-small cell lung cancer cell lines, and 5 cell lines had higher expression and enhanced phosphorylation of cMet. In the other five types, expression was weak and phosphorylation was low. When HGF was added, phosphorylation was enhanced in the Met-highly expressing cell line, but it disappeared in a short time. The effect of Met inhibitor was correlated with Met expression and phosphorylation status. Analysis of the downstream signals under HGF stimulation revealed that HGF stimulation increased the expression of 29 genes and decreased 138 genes. To date, we have collected tumor samples and clinical information for non-small cell lung cancer, but this study did not reveal a relationship between cMet and prognosis.

Free Research Field

呼吸器内科学

Academic Significance and Societal Importance of the Research Achievements

我々は、非小細胞肺癌細胞株を用いてcMet発現、リン酸化を検討したところ、5細胞我々は、非小細胞肺癌細胞株を用いcMet発現、リン酸化を検討したところ、5細胞株で高発現、リン酸化亢進を認めた。他の5種類では発現は弱くリン酸化も低かった。HGFを添加したところMet高発現細胞株でリン酸化亢進が認めたが、短時間で消失した。Met阻害剤の効果はMet発現とリン酸化状態に相関した。HGF刺激の元で下流シグナルを解析すると、HGF刺激で29遺伝子が発現増加し，138遺伝子は低下した。現在までに非小細胞肺癌の腫瘍検体と臨床情報を集積したが、今回の研究ではcMetと予後との関連は明らかにはならなかった。