KLF5 promotes proliferation in gastric cancer via regulating p21 and CDK4.

OBJECTIVE: This study aims to investigate the expression characteristics of Kruppel-like factor 5 (KLF5) in gastric cancer (GC) and its potential correlation to pathological indexes in GC patients. Molecular mechanisms underlying the regulatory effect of KLF5 on GC progression are explored. PATIENTS AND METHODS: KLF5 expressions in GC tissues were analyzed through GE-PIA dataset and those collected in our hospital. By analyzing the clinical data of GC patients, the correlation between KLF5 level and pathological characteristics of GC was determined. The regulatory effects of KLF5 on proliferative ability and cell cycle progression of SGC7901 and MGC803 cells were assessed by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry. The regulation of KLF5 on expression levels of p21 and CDK4 in GC cells was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. RESULTS: KLF5 was markedly upregulated in GC tissues. KLF5 level was positively correlated to TNM staging, tumor size, and metastasis of GC. Meanwhile, high level of KLF5 predicted poor prognosis in GC patients. The knockdown of KLF5 in SGC7901 and MGC803 cells attenuated proliferative ability and arrested cell cycle in G0/G1 phase. Both mRNA and the protein levels of p21 were upregulated, and CDK4 levels were downregulated in SGC7901 and MGC803 cells transfected with si-KLF5. CONCLUSIONS: KLF5 is upregulated in GC and closely linked to pathological characteristics of GC patients. High level of KLF5 indicates poor prognosis of GC. It is believed that KLF5 may be a potential therapeutic target for GC.