Background
Kinesin family member C3 (KIFC3), as reported, plays important roles in several tumor types. Nevertheless, it is unknown whether KIFC3 has effects on non-small cell lung cancer (NSCLC) development. Materials and
Conclusions
KIFC3 lack suppressed the proliferation, invasion, and migration which works, at least partially, by the PI3K/Akt pathway. These findings suggest that targeting KIFC3 via the PI3K/Akt pathway may offer a novel therapeutic strategy for NSCLC.
Methods
KIFC3 expression was detected by RT-PCR, and its correlation with prognosis was analyzed by GEPIA website. Small interfering RNA against KIFC3 were adopted for modulating KIFC3 expression in NSCLC cells. KIFC3 effects on NSCLC cell proliferation were determined using the MTT and clone formation assay. Matrigel invasion and wound healing assays were adopted for measuring the invasion and migration capability of NSCLC cells. Western blot was applied for measuring the levels of proteins associated with the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) pathway in NSCLC cells.
Results
KIFC3 was markedly increased in NSCLC samples and cells. KIFC3 knockdown suppressed the proliferation, invasion, and migration in NSCLC. Mechanically, KIFC3 silencing suppressed NSCLC progression through inhibiting the PI3K/Akt pathway. Conclusions: KIFC3 lack suppressed the proliferation, invasion, and migration which works, at least partially, by the PI3K/Akt pathway. These findings suggest that targeting KIFC3 via the PI3K/Akt pathway may offer a novel therapeutic strategy for NSCLC.