Proliferation by the autocrine signals AprA and CfaD, but that AprA and CfaD function in other processes that do not require BzpN. An important but unanswered question is how the putative transcription factor activity of BzpN might be altering gene expression to regulate cell proliferation. The tractability of Dictyostelium genetics may be useful in identifying potentially conserved genes that are upregulated or downregulated in response to BzpN activity that function to regulate proliferation, which may reveal novel BEZ235 approaches to reduce the proliferation of cancers. Ovarian cancer, the most lethal gynecological cancer and second only to endometrial cancer in the number of female reproductive track and organ cases diagnosed, led to approximately 21,880 new cases in the U.S. in 2010 with about 13,850 deaths. The high morbidity is attributable in large part to a lack of specific symptoms, thus delaying prognosis until advanced stages of the disease. The 5-year survival rate of ovarian cancer in later stages is 16�?8% according to the International Federation of Gynecology and Obstetrics. Consequently, the majority of ovarian cancer research has been focused on discovering screening methods for early diagnosis and identifying the possible contributing factors for prevention of the disease. A high correlation between ovarian cancer risk and altered reproductive cycles has been reported in many clinical studies. For example a higher risk is associated with peri- or post-menopause and incidences of infertility, while a decreased risk correlates with pregnancy, oral contraceptive use, hysterectomy and tubal ligation. In addition, the elevated level of the gonadotropins, luteinizing hormone and follicle-stimulating hormone, was consistently found in cysts and the peritoneal fluid of patients with ovarian cancer or borderline ovarian tumors, compared to benign cysts or benign tumors, which has attracted considerable attention, along with the status of the LH receptor, a member of the G proteincoupled receptor family, in the cancer. There are suggestions that LH could potentially serve as a cause or contributory factor to the development or progression of ovarian cancer, while other clinical reports show that there are no clear trends that using gonadotropins to treat infertility will increase the risk of ovarian cancer. With such controversy, elucidation of the downstream processes of LHR is imperative to discerning the ramifications of increasing levels of LH in LHR+ cancer cells. We have reported earlier that the phenotypes of the LHR+ cells, but not the LHR- cells, exhibited reduced proliferation, migratory and invasive properties in response to LH, and have shown elsewhere the consequent changes in transcriptomic level expression. The present study is focused on elucidating the effects of LH on microRNA expression and regulation.