Chemotherapy for Prostate Cancer

Dyrstad, Sara W.; Shah, Prabodh; Rao, K. Narasimha

doi:10.2174/138161206776056100

Cited by 12 publications

(15 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chemotherapy is currently one of the frequently used therapeutic strategies for prostate cancer [62][63][64], and measurement of EndoG may be a potentially useful approach to evaluate chemosensitivity of cancer cells to determine optimal conditions for chemotherapy. Manipulating with sensitivity to cytotoxic agents to alter cancer progression has been suggested as a therapeutic approach for prostate cancer in several studies [10,11].…”

Section: Discussionmentioning

confidence: 99%

Sensitivity of human prostate cancer cells to chemotherapeutic drugs depends on EndoG expression regulated by promoter methylation

et al. 2008

View full text Add to dashboard Cite

Analysis of promoter sequences of all known human cytotoxic endonucleases showed that endonuclease G (EndoG) is the only endonuclease that contains a CpG island, a segment of DNA with high G+C content and a site for methylation, in the promoter region. A comparison of three human prostate cancer cell lines showed that EndoG is highly expressed in 22Rv1 and LNCaP cells. In PC3 cells, EndoG was not expressed and the EndoG CpG island was hypermethylated.The expression of EndoG correlated positively with sensitivity to cisplatin and etoposide, and the silencing of EndoG by siRNA decreased the sensitivity of the cells to the chemotherapeutic agents in the two EndoG-expressing cell lines. 5-aza-2′-deoxycytidine caused hypomethylation of the EndoG promoter in PC3 cells, induced EndoG mRNA and protein expression, and made the cells sensitive to both cisplatin and etoposide. The acetylation of histones by trichostatin A, the histone deacetylase inhibitor, induced EndoG expression in 22Rv1 cells, while it had no such effect in PC3 cells. These data are the first indication that EndoG may be regulated by methylation of its gene promoter, and partially by histone acetylation, and that EndoG is essential for prostate cancer cell death in the used models.

show abstract

Section: Discussionmentioning

confidence: 99%

Sensitivity of human prostate cancer cells to chemotherapeutic drugs depends on EndoG expression regulated by promoter methylation

et al. 2008

View full text Add to dashboard Cite

show abstract

“…37,38). After establishment of visible tumors of f75 mm 3 , requiring f4 to 5 days, intratumoral injections of different adenoviruses were given only to the tumors on the left flank at a dose of 1 Â 10 8 plaqueforming units in 100 AL. No injection was given to the right-sided tumors.…”

Section: Methodsmentioning

confidence: 99%

“…To expand on the in vitro studies, in vivo assays were done using nude mice containing established DU-145-Bcl-x L s.c. xenografts on both right and left flanks. After palpable tumors of f75 mm 3 developed, in f4 to 5 days, seven intratumoral injections with different adenoviruses, thrice per week for the first week and twice per week for an additional 2 weeks, were administered to the tumors on the left flank at a dose of 1 Â 10 10 viral particles in 100 AL. No injections were given to the right-sided tumors.…”

Section: Cancer Researchmentioning

confidence: 99%

“…Hormonal treatment with antiandrogens is the standard therapy for stage IV prostate cancer, but patients ultimately become nonresponsive to androgen ablation (1,2). Current therapy options for patients with hormone-refractory prostate cancer include radiotherapy and cytotoxic chemotherapeutic agents, such as mitoxantrone, estramustine, and taxanes (1)(2)(3). Despite a palliative benefit, none of these approaches engender a beneficial effect on the overall survival of patients.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Eradication of Therapy-Resistant Human Prostate Tumors Using a Cancer Terminator Virus

Sarkar¹,

Lebedeva²,

Su³

et al. 2007

Cancer Research

View full text Add to dashboard Cite

Terminal prostate cancer is refractory to conventional anticancer treatments because of frequent overexpression of antiapoptotic proteins Bcl-2 and/or Bcl-x L . Adenovirus-mediated delivery of melanoma differentiation associated gene-7/ interleukin-24 (mda-7/IL-24), a secreted cytokine having cancer-selective apoptosis-inducing properties, profoundly inhibits prostate cancer cell growth. However, forced overexpression of Bcl-2 or Bcl-x L renders prostate cancer cells resistant to Ad.mda-7. We constructed a conditionally replication-competent adenovirus in which expression of the adenoviral E1A gene, necessary for replication, is driven by the cancer-specific promoter of progression elevated gene-3 (PEG-3) and which simultaneously expresses mda-7/IL-24 in the E3 region of the adenovirus (Ad.PEG-E1A-mda-7), a cancer terminator virus (CTV ). This CTV generates large quantities of MDA-7/IL-24 as a function of adenovirus replication uniquely in cancer cells. Infection of Ad.PEG-E1A-mda-7 (CTV) in normal prostate epithelial cells and parental and Bcl-2-or Bcl-x L -overexpressing prostate cancer cells confirmed cancer cell-selective adenoviral replication, mda-7/IL-24 expression, growth inhibition, and apoptosis induction. Injecting Ad.PEG-E1A-mda-7 (CTV ) into xenografts derived from DU-145-Bcl-x L cells in athymic nude mice completely eradicated not only primary tumors but also distant tumors (established in the opposite flank), thereby implementing a cure. These provocative findings advocate potential therapeutic applications of this novel virus for advanced prostate cancer patients with metastatic disease. [Cancer Res 2007;67(11):5434-42]

show abstract

“…Future studies may be necessary to determine the role of other epigenetic mechanisms in regulation of EndoG and their role in chemoresistance to prostate cancer and cancers of other organs. Chemotherapy is currently one of the frequently used therapeutic strategies for prostate cancer (Dyrstad et al, 2006;Kaku et al, 2006;Nakabayashi & Oh, 2006), and measurement of EndoG may be a potentially useful approach to evaluate chemosensitivity of cancer cells to determine optimal conditions for chemotherapy prior to the therapy. If further in vivo studies confirm our observation that EndoG is a potential key mediator of prostate cancer cell death regulated by the methylation of EndoG gene promoter, future epigenetic therapeutics will need to be targeted to EndoG.…”

Section: Conclusive Remarksmentioning

confidence: 99%