siRNA directed against survivin enhances pancreatic cancer cell gemcitabine chemosensitivity
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Updated: Jul 4, 2026

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
Published on: December 9, 2016
Wen-Song Liu1, Hai-Jiao Yan, Ren-Yi Qin
1Department of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
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.
Insights
RNA interference targeting survivin significantly reduced pancreatic cancer cell growth and increased apoptosis. This survivin suppression also enhanced chemotherapy effectiveness, suggesting a novel therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Survivin overexpression is common in human cancers, including pancreatic cancer.
- Survivin contributes to resistance against radiation and chemotherapy treatments.
- Targeting survivin presents a potential therapeutic strategy for pancreatic cancer.
Purpose of the Study:
- To investigate the efficacy of survivin-targeted short interfering RNA (siRNA) in human pancreatic cancer cells.
- To evaluate the impact of survivin suppression on cancer cell growth, apoptosis, and cell cycle.
- To determine if survivin inhibition enhances chemosensitivity to gemcitabine.
Main Methods:
- Construction and transfection of a survivin siRNA plasmid expression vector into Panc-1 and BxPC3 cell lines.
- Detection of survivin mRNA and protein levels using RT-PCR and Western blot.
- Assessment of cell growth, cell cycle distribution, apoptosis, and cytotoxicity via trypan blue exclusion, flow cytometry, and MTT assay.
Main Results:
- Survivin siRNA treatment led to a significant reduction in survivin mRNA and protein expression.
- Suppression of survivin resulted in decreased tumor cell growth, increased spontaneous apoptosis, and G0/G1 cell cycle arrest.
- Survivin suppression markedly enhanced the chemosensitivity of pancreatic cancer cells to gemcitabine.
Conclusions:
- RNA interference (RNAi) targeting the survivin gene is a viable strategy for inhibiting pancreatic cancer progression.
- Survivin suppression can overcome chemoresistance, offering a potential approach for chemosensitization therapy.
- Targeting survivin holds promise as an adjuvant therapy to improve pancreatic cancer treatment outcomes.
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