Knockdown of lncRNA MIR4435-2HG and ST8SIA1 expression inhibits the proliferation, invasion and migration of prostate cancer cells in vitro and in vivo by blocking the activation of the FAK/AKT/β-catenin signaling pathway

Prostate cancer is a main health risk for males with a high incidence and mortality. The present study aimed to examine the effects of long non-coding RNA (lncRNA) MIR4435-2HG binding with ST8SIA1 on the proliferation, invasion and migration of prostate cancer cells via the activation of the FAK/AKT/β-catenin signaling pathway. The expression of MIR4435-2HG and ST8SIA1 in prostate cancer cell lines, and the transfection efficacy were analyzed by RT-qPCR. The proliferation, clone formation ability, and the invasion and migration of transfected cells were detected by CCK-8 assay, clone formation assay, Transwell assay and wound healing assay, respectively. Plasmids were injected subcutaneously into mice to construct a xenograft tumor model. The expression levels of proteins related to proliferation, apoptosis, invasion and migration, and the FAK/AKT/β-catenin pathway were detected by western blot analysis. The results revealed that MIR4435-2HG expression was increased in the prostate cancer cell lines and MIR4435-2HG expression was the highest in the PC-3 cells. Interference with MIR4435-2HG inhibited the proliferation, clone formation ability, and the invasion and migration of PC-3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/β-catenin signaling pathway. MIR4435-2HG was demonstrated to target ST8SIA1. ST8SIA1 expression was also increased in the prostate cancer cell lines and MIR4435-2HG expression was the highest in the PC-3 cells. Interference with ST8SIA1 inhibited the promoting effects of MIR4435-2HG on the proliferation, invasion and migration of PC-3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/β-catenin signaling pathway. On the whole, the present study demonstrates that interference with MIR4435-2HG, combined with ST8SIA1, inhibits the proliferation, invasion and migration of prostate cancer cells in vitro and in vivo by blocking the activation of the FAK/AKT/β-catenin signaling pathway.