Inhibited cell proliferation and induced apoptosis in vitro and in vivo. Reduce tumor progression via apoptosis. Reduced tumor weight. Increased expression of Bax, cleaved caspase-3, and reduction in Bcl-2 expression. No cytotoxic effect in T98G. Apoptosis induced via increased expression of estrogen receptor β and p53 [357]. The gene discussed is BCL2; the disease is neoplasm.