ArticleThe Prostate2005
Antisense Bcl-2 sensitizes prostate cancer cells to radiation.
Article in The Prostate, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 53 citations in OpenAlex.
- Bcl-2 and Bax expression predict prostate cancer outcome in men treated with androgen deprivation and radiotherapy on radiation therapy oncology group protocol 92-02.Clinical cancer research : an official journal of the American Association for Cancer Research · 2007Trial
- Article
- Novel Apoptosis-Inducing Agents for the Treatment of Cancer, a New Arsenal in the Toolbox.Cancers · 2019Review
- Tumor-Specific Induction of the Intrinsic Apoptotic Pathway-A New Therapeutic Option for Advanced Prostate Cancer?Frontiers in oncology · 2019Article
- Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Manipulating the apoptotic pathway: potential therapeutics for cancer patients.British journal of clinical pharmacology · 2013Review
- Increased expression of the androgen receptor with p300 and interleukin-6 coactivators compensate for oligonucleotide suppression of bcl-2: no increased CREB binding protein or interleukin-4 expression.Therapeutic advances in urology · 2013Article
- Oligonucleotide suppression of bcl-2 in LNCaP cells is compensated by increased androgen sensitivity, p53 and oncogene activity, and suppressed caspase-3.Medical oncology (Northwood, London, England) · 2013Article
- Compensatory and non-compensatory effects on protein expression following BCL-2 suppression by antisense oligonucleotides.Medical oncology (Northwood, London, England) · 2012Article
- In LNCaP cells enhanced expression of both androgen receptor and costimulatory protein p300 compensate for antisense oligonucleotide suppression of bcl-2.Therapeutic advances in urology · 2011Article
- Bax expression remains unchanged following antisense treatment directed against BCL-2.Medical oncology (Northwood, London, England) · 2011Article
- In LNCaP cells enhanced expression of the androgen receptor compensates for Bcl-2 suppression by antisense oligonucleotides.Therapeutic advances in urology · 2011Article
- Acid ceramidase upregulation in prostate cancer cells confers resistance to radiation: AC inhibition, a potential radiosensitizer.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
- Antisense MDM2 enhances E2F1-induced apoptosis and the combination sensitizes androgen-sensitive [corrected] and androgen-insensitive [corrected] prostate cancer cells to radiation.Molecular cancer research : MCR · 2008Article
- Adenovirus-mediated restoration of expression of the tumor suppressor gene DLC1 inhibits the proliferation and tumorigenicity of aggressive, androgen-independent human prostate cancer cell lines: prospects for gene therapy.Cancer gene therapy · 2008Article
- Antisense MDM2 enhances the response of androgen insensitive human prostate cancer cells to androgen deprivation in vitro and in vivo.The Prostate · 2008Article
- Modulation of tumor radiation response with G3139, a bcl-2 antisense oligonucleotide.Investigational new drugs · 2007Article
- No supra-additive effects of goserelin and radiotherapy on clonogenic survival of prostate carcinoma cells in vitro.Radiation oncology (London, England) · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBcl-2 is anti-apoptotic and overexpression is associated with prostate tumor aggressiveness. We hypothesized that Bcl-2 has a role in prostate cancer radiation (RT) response. The relationship of Bcl-2 expression in four prostate cancer cell lines, and the effect of modulating expression with a Bcl-2 antisense oligonucleotide (G3139, Genasense, oblimersen sodium, Genta Incorporated), to RT was examined.
methodsThe four cell lines studied were LNCaP (wild type-p53), PC3 (p53 null), Bcl-2 stably transfected LNCaP (LNCaP-BST), and Bcl-2 stably transfected PC3 (PC3-BST) cells. Cells were treated with antisense (AS) Bcl-2 alone or with RT (2-6 Gy). Following RT, cells were processed at 3-6 hr for Western blots, 18 hr for Annexin V staining and flow cytometric analysis, 24 hr for caspases 3+7 quantification by fluorometric assay, and immediately for clonogenic survival.
resultsAS caused a significant reduction in Bcl-2 expression in all cell lines. P53 expression was elevated following RT treatment in LNCaP and LNCaP-BST cells. P21 was increased by RT treatment in all cell lines. AS caused a significant increase in caspase 3+7 activity over the mismatch (MM) controls in all cell lines. When AS was combined with RT, caspase 3+7 activity was further increased significantly over all other groups in all cell lines. Moreover, AS+RT resulted in significantly reduced clonogenic survival over MM+RT, which was dampened in the Bcl-2 overexpressing lines.
conclusionsTo our knowledge, these data demonstrate for the first time that a Bcl-2 specific AS oligonucleotide sensitizes prostate cancer cells to RT. p53 is not required for this effect.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.