KIF4A knockdown inhibits tumor progression and promotes chemo-sensitivity via induction of P21 in lung cancer cells

KIF4A has been demonstrated to play a crucial function in the pathogenesis of a broad number of tumors and have close association with PI3K/AKT pathway. The aim of this study was to explore the potential function of KIF4A in lung cancer progression by targeting PI3K/AKT pathway and P21 combination with doxorubicin. A549 cell lines were transfected with siRNA against KIF4A and negative control siRNA (si-NC). MTT assay and trypan blue staining were used to evaluate the effect of si-KIF4A on the doxorubicin cytotoxicity. The mRNA and protein expression levels of KIF4A and p21 were assessed by qRT-PCR and Western blotting. Apoptosis was measured by cell death ELISA kit. Our result revealed that KIF4A silencing decreased cellular proliferation in A549 lung cancer cells. Doxorubicin in combination with si-KIF4A led to significant reduction in the survival rate of A549 cell. KIF4A silencing upregulated p21. In conclusion, our results demonstrate that KIF4A inhibition sensitizes A549 cells to doxorubicin by targeting p21 and PI3K/AKT pathway, indicating a significant role for KIF4A in lung cancer chemotherapy.

Automated summary

This study reveals the significant role of KIF4A in lung cancer progression, and demonstrates that KIF4A inhibition can enhance the sensitivity of lung cancer cells to doxorubicin through targeting p21 and PI3K/AKT pathway.