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Erschienen in: Digestive Diseases and Sciences 1/2009

01.01.2009 | Original Article

siRNA Directed Against Survivin Enhances Pancreatic Cancer Cell Gemcitabine Chemosensitivity

verfasst von: Wen-Song Liu, Hai-Jiao Yan, Ren-Yi Qin, Rui Tian, Min Wang, Jian-Xin Jiang, Ming Shen, Cheng-Jian Shi

Erschienen in: Digestive Diseases and Sciences | Ausgabe 1/2009

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Abstract

Survivin is known to be overexpressed in various human malignancies, including pancreatic cancer, and to cause resistance to radiation and chemotherapy, so the regulation of this molecule could be a new strategy for treating pancreatic cancer. In our study, a short interfering RNA (siRNA) plasmid expression vector against survivin was constructed and transfected into human pancreatic cancer cell lines of Panc-1 and BxPC3. The expression of survivin mRNA and protein among the stable transfected cells and the untransfected cells was detected by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot, respectively. Tumor cell growth in vitro was assessed by trypan blue exclusion. The cell cycle distribution and cell apoptosis were measured by flow cytometry. The cytotoxicity assay was measured by the MTT test. Our results showed that survivin siRNA treatment caused a specific and profound decrease of survivin mRNA and protein that was associated with decreased cell growth, spontaneous apoptosis, and a specific G0/G1 arrest. Furthermore, the suppression of survivin can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine significantly. We suggest that the RNAi against survivin gene strategy would be a potential approach to chemosensitization therapy in human pancreatic cancer.
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Metadaten
Titel
siRNA Directed Against Survivin Enhances Pancreatic Cancer Cell Gemcitabine Chemosensitivity
verfasst von
Wen-Song Liu
Hai-Jiao Yan
Ren-Yi Qin
Rui Tian
Min Wang
Jian-Xin Jiang
Ming Shen
Cheng-Jian Shi
Publikationsdatum
01.01.2009
Verlag
Springer US
Erschienen in
Digestive Diseases and Sciences / Ausgabe 1/2009
Print ISSN: 0163-2116
Elektronische ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-008-0329-4

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