%0 Journal Article
%T Possible immunotherapeutic potentiation with D-Fraction in prostate cancer cells
%A Paul Pyo
%A Brandon Louie
%A Srinivas Rajamahanty
%A Muhammad Choudhury
%A Sensuke Konno
%J Journal of Hematology & Oncology
%D 2008
%I BioMed Central
%R 10.1186/1756-8722-1-25
%X Potential effects of recombinant IFN-¦Á2b (0¨C100,000 IU/ml), PDF (0¨C1,000 ¦Ìg/ml), or their combinations were assessed on the growth of PC-3 cells at 72 h. Cell cycle analysis using a flow cytometer and Western blot analysis were performed to explore antiproliferative mechanism of these agents. The dose-dependent study showed that IFN-¦Á2b up to 20,000 (20 K) IU/ml had no significant effects, but >60% growth reduction was attained ¡Ü50 K IU/ml. Similarly, PDF showed no effects up to 250 ¦Ìg/ml but ~65% growth reduction was seen at 1,000 ¦Ìg/ml. When IFN-¦Á2b and PDF were combined, a relatively low concentration (10 K IU/ml) of IFN-¦Á2b and PDF (250 ¦Ìg/ml) resulted in a ~65% growth reduction. This was accompanied by a G1 cell cycle arrest, indicated by cell cycle analysis. Western blots also revealed that the G1-specific cell cycle regulators, CDK2, CDK4, CDK6, cyclin D1, and cyclin E, had been significantly (>60%) down-regulated in IFN/PDF-treated cells.The combination of IFN-¦Á2b (10 K IU/ml) and PDF (250 ¦Ìg/ml) is capable of inducing a ~65% reduction in PC-3 cell growth. This appears to be due to a synergistic potentiation of two agents, leading to a G1 cell cycle arrest. Thus, it is conceivable that PDF may potentiate IFN-¦Á2b activity, improving immunotherapy for prostate cancer.Current therapy for prostate cancer (CaP), the most common malignancy in elderly men in the United States [1], is directed at exploitation of the androgen-dependent state of prostatic cancer cells. Various antiandrogens and leuteinizing hormone-releasing hormone (LHRH) agonists are useful for blocking the availability of androgen to the cancer cells [2]. However, the efficacy of these drugs is of limited duration, and patients experience an almost inevitable progression of their cancers to the fatal androgen-independent state [3]. To develop an alternative approach for controlling or preventing such disease progression, it demands in searching for agents/drugs that could effectively regulate the C
%U http://www.jhoonline.org/content/1/1/25