Extracellular chaperonin 10 augments apoptotic cell death induced by 5-fluorouracil in human colon cancer cells
- Authors
- Kim, Kun; Yeo, Seung-Gu
- Issue Date
- Nov-2014
- Publisher
- II Pensiero Scientifico Editore srl
- Keywords
- 5-fluorouracil; colon cancer; chaperonin; drug resistance
- Citation
- Tumori, v.100, no.6, pp E230 - E235
- Journal Title
- Tumori
- Volume
- 100
- Number
- 6
- Start Page
- E230
- End Page
- E235
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/11753
- DOI
- 10.1177/1778.19282
- ISSN
- 0300-8916
2038-2529
- Abstract
- Aims and background. The molecular mechanisms involved in resistance to 5-fluorouracil (5-FU) in colon cancer patients remain to be elucidated. The purpose of this study was to identify proteins associated with 5-FU resistance in colon cancer. Methods and study design. Proteins secreted from a 5-FU-resistant human colon cancer cell line (SNU-C4 5-FU 200) were analyzed by two-dimensional gel electrophoresis- based proteomics, and identified using matrix-associated laser desorption/ionization-mass spectroscopy analysis and SWISS-PROT database searches. The expression levels of candidate proteins were determined by Western blotting and cell proliferation was monitored by MTT assay. Results. Chaperonin 10 (cpn10) was secreted at a lower level by 5-FU-resistant cells compared to the non-resistant parent cell line. The proliferation of both the parent and 5-FU-resistant cell lines increased slightly when extracellular cpn10 alone was added. However, in the presence of 5-FU, cpn10 augmented 5-FU-induced apoptotic death in both cell lines. Cpn10 led to activation of extracellular signal-regulated kinase 1/2 (ERK 1/2), and a specific ERK 1/2 inhibitor, PD98059, completely inhibited cpn10-stimulated cell proliferation. Conclusions. Our findings indicate that concurrent treatment with cpn10 and 5-FU warrants further investigation in an effort to overcome 5-FU resistance and enhance the efficacy of 5-FU therapy for colon cancer.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Medicine > Department of Radiation Oncology > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.