Prostate cancer have been most cause of cancer death to men in recent, but there are not effective treatments for this cancer. In growth of prostate cancer, steroid hormones such as androgen play a role in their growth and survival. However, endocrine disrupting chemicals (EDCs) intend to bind the hormone receptor and induce the abnormal hormone response. EDCs have potency to activate estrogen receptor (ER) and androgen receptor (AR) mediated signaling pathways, and they cause the human health problem including hormone-dependent carcinogenesis. Bisphenol A (BPA) has the phenolic structure with the effect on the endocrine system and promotes human breast cancer. Recent studies have reported that phthalates have a potency to disrupt reproductive system in male rodents. Thus, we identified in this study whether BPA and dibutyl phthalate (DBP) stimulate the cell growth of prostate cancer cells, LNCaP cells, which have both ERs and ARs. We evaluated proliferation of LNCaP cells following BPA and DBP treatment using a cell viability assay. Both BPA and DBP promoted LNCaP cells proliferation over two-fold at 10−7 M to 10−5 M compared to a vehicle. Further, we examined the alteration of the downstream target genes of ras signaling pathways by using the semi-quantitative RT-PCR. Like 17b-estradiol (E2) and dihydrotestosterone (DHP), the treatments with BPA and DBP resulted in a significant increase in the transcriptional levels of c-myc and c-fos in LNCaP cells at 30 min to 6 h, compared to a vehicle. In addition, these EDCs induced cyclin D1, a cell cycle related gene, at 6 h after treatment. Taken together, these results suggest that BPA and phthalate can alter gene expressions of downstream targets associated with ras signaling and cell cycle related pathways in prostate cancer cells. A novel effect of EDCs may result in the cell growth of human prostate cancer cells. A further study warranties to determine the potential of EDCs in the carcinogenesis of prostate cancer. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of Korea government (no. 2011-0015385).
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details unavailable.