Role of FBXO17 in EGFR mutation positive NSCLC

Research Project

Project/Area Number	26860614
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Respiratory organ internal medicine
Research Institution	Keio University
Principal Investigator	HAMAMOTO JUNKO 慶應義塾大学, 医学部, 特任助教 (40570239)
Project Period (FY)	2014-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000) Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	EGFR / FBXO17 / 肺癌
Outline of Final Research Achievements	We found that knockdown of FBXO17 induced cell growth arrest in 6 lung cancer cell lines out of tested 8 cell lines. Not all but some lung cancer cell lines showed up-regulation of phosphorylated ERK by FBXO17 overexpression. Moreover, G1/S cell cycle checkpoint was disrupted by FBXO17 overexpression in all tested lung cancer cell lines. We could not identify the binding protein of FBXO17, but we've suggested that FBXO17 is an important gene implicating in cell growth, cell cycle and EGFR pathway.

Report

(3 results)