Functional and pathway analyses suggested multiple molecular mechanisms for estrogen-dependent growth of human uterine fibroids: enhanced tumor cell survival by increased expression of PCP4 and decreased expression of TGF-β R2 and PTGER3 and the complex interplay among five distinct nuclear receptors (ER, RAR, RXR, NR4A1 and PPARγ) that may enhance tumor cell survival and growth. The gene discussed is PTGER3; the disease is neoplasm.