Accumulating data has demonstrated that the silencing of Lgr5 influences the functional and molecular outcome of colorectal cancer cells, breast cancer cells, cervical cancer and ovarian cancer [25, 43, 46–47]; for example, previous reports indicated that knocking down endogenous Lgr5 in cultured colorectal cancer cell lines reduced their proliferation, migration, invasion, growth rates and colony formation capability. This evidence concerns the gene LGR5 and ovarian cancer.