FOXK 2 is highly expressed in gastric carcinoma , and facilitates cells proliferation through transcriptional inhibition of CHEK 2 and promotes metastasis

FOXK2, as a transcription factor, plays crucial function in multiple cancers, but its role in gastric carcinoma (GC) is still unknown. We aim to evaluate the function of FOXK2 in GC. In this study, we first performed qRT-PCR and western blotting to detect the expression of FOXK2 in GC. The results indicated that FOXK2 was highly expressed in GC. Moreover, high expression of FOXK2 was positively correlated with tumor size, clinical stages, metastasis and poor prognosis. Several functional experiments, including colony formation assay and CCK-8 assay, revealed that FOXK2 can promote cell proliferation in GC. In addition, cell cycle analysis demonstrated FOXK2 also regulated cell cycle through regulation of CHEK2. Luciferase reporter analysis and ChIP analysis confirmed that FOXK2 transcription suppressed CHEK2. Western blot and qRT-PCR showed FOXK2 promoted EMT, high expression of FOXK2 was correlated with loss of E-cadherin expression, and gain of N-cadherin and Vimentin expression. Our work showed as an oncogene, FOXK2 facilitated cell proliferation and metastasis through regulation of cell cycle and EMT in GC, and we provided FOXK2 as a novel molecular therapy target.