HSP72 interactome identifies key molecules for intrinsic resitance to gemcitabine in pancreatic cancer

2015 Fiscal Year Final Research Report

• Project/Area Number: 26890021
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Tumor therapeutics
• Research Institution: Osaka City University
• Principal Investigator: Tanaka Masako (橘昌子) 大阪市立大学, 大学院医学研究科, 特任助教 (00733651)
• Project Period (FY): 2014-08-29 – 2016-03-31
• Keywords: 薬剤耐性 / 熱ショックタンパク質 / インタラクトーム / 膵癌

Outline of Final Research Achievements

We established cell lines tolerant to serum starvation (PANC-1/Stv) and hypoxia (PANC-1/Hyp) from the parental cell line PANC-1. The IC50 values of gemcitabine for PANC-1/Stv and PANC-1/Hyp cells (under non-stressful conditions) was 142- and 37-fold higher, respectively, than that for the parental cells. These cell lines developed this resistance to gemcitabine via suppression of apoptosis, which is a mechanism of resistance that is common to that of the cell line (PANC-1/GEM) with acquired gemcitabine resistance. However, drug resistance in PANC-1/GEM cells was primarily caused by gemcitabine inactivation. We then compared HSP72 interactome of PANC-1/GEM cells to PANC-1/Stv and PANC-1/Hyp cells, resulting in identification of 37 molecules unique to intrinsic resistance to gemcitabine.

Free Research Field

分子薬理学