atpenin-a4 and Prostatic-Neoplasms

atpenin-a4 has been researched along with Prostatic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for atpenin-a4 and Prostatic-Neoplasms

ArticleYear
Leucinostatin A inhibits prostate cancer growth through reduction of insulin-like growth factor-I expression in prostate stromal cells.
    International journal of cancer, 2010, Feb-15, Volume: 126, Issue:4

    Targeting stroma in tumor tissues is an attractive new strategy for cancer treatment. We developed in vitro coculture system, in which the growth of human prostate cancer DU-145 cells is stimulated by prostate stromal cells (PrSC) through insulin-like growth factor I (IGF-I). Using this system, we have been searching for small molecules that inhibit tumor growth through modulation of tumor-stromal cell interactions. As a result, we have found that leucinostatins and atpenins, natural antifungal antibiotics, inhibit the growth of DU-145 cells cocultured with PrSC more strongly than that of DU-145 cells alone. In this study we examined the antitumor effects of these small molecules in vitro and in vivo. When DU-145 cells were coinoculated with PrSC subcutaneously in nude mice, leucinostatin A was found to significantly suppress the tumor growth more than atpenin B. The antitumor effect of leucinostatin A in vivo was not obtained against the tumors of DU-145 cells alone. RT-PCR experiments revealed that leucinostatin A specifically inhibited IGF-I expression in PrSC without effect on expressions of other IGF axis molecules. Leucinostatins and atpenins are known to abrogate mitochondrial functions. However, when we used mitochondrial DNA-depleted, pseudo-rho(0) cells, we found that one of leucinostain A actions certainly depended on mitochondrial function, but it actually inhibited the growth of DU-145 cells more strongly in coculture with pseudo-rho(0) PrSC and reduced IGF-I expression in pseudo-rho(0) PrSC. Taken together, our results suggested that leucinostatin A inhibited prostate cancer cell growth through reduction of IGF-I expression in PrSC.

    Topics: Animals; Antimicrobial Cationic Peptides; Antineoplastic Agents; Cell Division; Cell Line, Tumor; Coculture Techniques; DNA Primers; Humans; Male; Mice; Mice, Nude; Mitochondria; Mycotoxins; Peptides; Prostatic Neoplasms; Pyridones; Reverse Transcriptase Polymerase Chain Reaction; Stromal Cells

2010