Knockdown survivin expression reduces the efficacy of curcumin treatment in hepatocellular carcinoma cells.

Abstract

BACKGROUND:

Survivin is a potential therapeutic target for cancer. Increased survivin expression promotes cell survival and therapeutic resistance. However, there is little information regarding whether the expression level of survivin affects curcumin treatment in hepatocellular carcinoma (HCC).

METHODS:

Survivin expression was suppressed in HCC cells using a short interfering RNA (siRNA) technique. The anticancer effects of curcumin were examined using a biosensor system, MTT assay, TUNEL assay, and cell cycle analysis.

RESULTS:

Curcumin resistance developed in cells with suppressed survivin, in contrast to the parental cells, as determined by survival assays. Cell cycle analysis and TUNEL assays revealed that the apoptotic cell population was increased in the scrambled-siRNA cells treated with curcumin compared with the survivin-siRNA cells. Suppression of survivin expression resulted in curcumin resistance via the modulation of Bcl-2 and Bax expression.

CONCLUSIONS:

We conclude that the expression levels of survivin may mediate the therapeutic efficacy of curcumin in HCC cells.

• Authors: Chin-Sheng Hung, Hui-Hsiung Liu, Ming-Te Huang, Chao-Wen Cheng, Li-Jen Kuo, Yuan-Soon Ho, Chih-Hsiung Wu, Chien-Ming Chen, Po-Li Wei, Yu-Jia Chang
• Journal: Annals of surgical oncology (Ann Surg Oncol) Vol. 19 Issue 11 Pg. 3547-55 (Oct 2012) ISSN: 1534-4681 [Electronic] United States
• PMID: 22711176 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• BIRC5 protein, human
• Inhibitor of Apoptosis Proteins
• Proto-Oncogene Proteins c-bcl-2
• RNA, Small Interfering
• Survivin
• bcl-2-Associated X Protein
• Curcumin

Topics

• Antineoplastic Agents (therapeutic use)
• Apoptosis (drug effects)
• Carcinoma, Hepatocellular (drug therapy, metabolism)
• Cell Cycle Checkpoints (drug effects)
• Cell Survival (drug effects)
• Curcumin (therapeutic use)
• Drug Resistance, Neoplasm
• Hep G2 Cells
• Humans
• Inhibitor of Apoptosis Proteins (genetics, metabolism)
• Liver Neoplasms (drug therapy, metabolism)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• RNA Interference
• RNA, Small Interfering (genetics, pharmacology)
• Survivin
• bcl-2-Associated X Protein (metabolism)