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