Derdak, Z; Mark, N.M.; Beldi, G; Robson, S.C.; Wands, J.R.; Baffy, G (2008). The mitochondrial uncoupling protein-2 promotes chemoresistance in cancer cells. Cancer research, 68(8), pp. 2813-9. Birmingham, Ala.: American Association for Cancer Research AACR 10.1158/0008-5472.CAN-08-0053
Full text not available from this repository. (Request a copy)Cancer cells acquire drug resistance as a result of selection pressure dictated by unfavorable microenvironments. This survival process is facilitated through efficient control of oxidative stress originating from mitochondria that typically initiates programmed cell death. We show this critical adaptive response in cancer cells to be linked to uncoupling protein-2 (UCP2), a mitochondrial suppressor of reactive oxygen species (ROS). UCP2 is present in drug-resistant lines of various cancer cells and in human colon cancer. Overexpression of UCP2 in HCT116 human colon cancer cells inhibits ROS accumulation and apoptosis after exposure to chemotherapeutic agents. Tumor xenografts of UCP2-overexpressing HCT116 cells retain growth in nude mice receiving chemotherapy. Augmented cancer cell survival is accompanied by altered NH(2)-terminal phosphorylation of the pivotal tumor suppressor p53 and induction of the glycolytic phenotype (Warburg effect). These findings link UCP2 with molecular mechanisms of chemoresistance. Targeting UCP2 may be considered a novel treatment strategy for cancer.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Visceral Surgery |
UniBE Contributor: |
Beldi, Guido Jakob Friedrich |
ISSN: |
0008-5472 |
ISBN: |
1538-7445 (Electroni |
Publisher: |
American Association for Cancer Research AACR |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:04 |
Last Modified: |
05 Dec 2022 14:19 |
Publisher DOI: |
10.1158/0008-5472.CAN-08-0053 |
Web of Science ID: |
000255100500033 |
URI: |
https://boris.unibe.ch/id/eprint/27696 (FactScience: 110169) |
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