ArticleJournal of cancer research and clinical oncology2011
Therapeutic effects of survivin dominant negative mutant in a mouse model of prostate cancer.
Article in Journal of cancer research and clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Nucleic acid cancer vaccines targeting tumor related angiogenesis. Could mRNA vaccines constitute a game changer?Frontiers in immunology · 2024Review
- In vivo antitumor activity of liposome‑plasmid DNA encoding mutant survivin‑T34A in cervical cancer.Molecular medicine reports · 2018Article
- Nintedanib antiangiogenic inhibitor effectiveness in delaying adenocarcinoma progression in Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP).Journal of biomedical science · 2017Article
- Efficient inhibition of ovarian cancer by degradable nanoparticle-delivered survivin T34A gene.International journal of nanomedicine · 2016Article
- Synergistic effects of eukaryotic coexpression plasmid carrying LKB1 and FUS1 genes on lung cancer in vitro and in vivo.Journal of cancer research and clinical oncology · 2014Article
- Functional promoter -31G/C variant of Survivin gene predict prostate cancer susceptibility among Chinese: a case control study.BMC cancer · 2013Article
- Gene therapy for C-26 colon cancer using heparin-polyethyleneimine nanoparticle-mediated survivin T34A.International journal of nanomedicine · 2011Article
- Survivin-T34A: molecular mechanism and therapeutic potential.OncoTargets and therapy · 2010Article
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Authors and funding
16 authors.
Funding
Abstract
purposePatients with localized prostate cancer can usually achieve initial response to conventional treatment. However, most of them will inevitably progress to advanced disease stage. There is a clear need to develop innovative and effective therapeutics for prostate cancer. Mouse survivin T34A (mS-T34A) is a phosphorylation-defective Thr34 → Ala dominant negative mutant, which represents a potential promising target for cancer gene therapy. This study was designed to determine whether mS-T34A plasmid encapsuled by DOTAP-chol liposome (Lip-mS) has the anti-tumor activity against prostate cancer, if so, to further investigate the possible mechanisms.
methodsIn vitro, TRAMP-C1 cells were transfected with Lip-mS and examined for apoptosis by PI staining and flow cytometric analysis. In vivo, subcutaneous prostate cancer models were established in C57BL/6 mice, which were randomly assigned into three groups to receive i.v. administrations of Lip-mS, pVITRO2-null plasmid complexed with DOTAP-chol liposome (Lip-null) or normal saline every 2 days for eight doses. Tumor volume was measured. Tumor tissues were inspected for apoptosis by TUNEL assay. Microvessel density (MVD) was determined by CD31 immunohistochemistry. Alginate-encapsulated tumor cell test was conducted to evaluate the treatment effect on angiogenesis.
resultsAdministration of Lip-mS resulted in significant inhibition in the growth of mouse TRAMP-C1 tumors. The anti-tumor response was associated with increased tumor cell apoptosis and decreased microvessel density.
conclusionsThe present study may be of importance in the exploration of the potential application of Lip-mS in the treatment of a broad spectrum of tumors.
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