Long non-coding RNA AFAP1-AS1 promotes proliferation and migration of gastric cancer by downregulating KLF2

X.-H. Yuan, J. Li, Y. Cao, Z.-G. Jie, Y.-F. Zeng

Department of General Surgery, Jiangxi provincial People’s Hospital Affiliated to Nanchang University, Nanchang, Chinajiezg123@126.com

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• Oncology

OBJECTIVE:  To clarify the function of actin filament associated protein 1-antisense RNA1 (AFAP1-AS1) to promote the proliferation and migration of gastric cancer (GC) cells by downregulating Krüppel-like factor 2 (KLF2).

MATERIALS AND METHODS: Expression level of AFAP1-AS1 in GC tissues and matched paracancerous tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Besides, its level in GC either with lymphatic metastasis or not, and those in different tumor stages were determined as well. Regulatory roles of AFAP1-AS1 in cellular behaviors of GC cells were evaluated by functional experiments. The ability of AFAP1-AS1 to recruit EZH2 was evaluated through chromatin immunoprecipitation (ChIP) assay. The expression level of KLF2 in GC cells influenced by AFAP1-AS1 and EZH2 was detected by Western blot. Finally, a series of rescue experiments were conducted to clarify the role of AFAP-AS1/KLF2 in GC cell performances.

RESULTS: AFAP1-AS1 was upregulated in GC tissues, and its expression in lymph node metastasis and progressive gastric cancer tissues were much higher. Knockdown of AFAP1-AS1 reduced the viability, proliferative and migratory abilities, but induced apoptosis of GC cells. AFAP1-AS1 was verified to bind to EZH2. After knockdown of AFAP1-AS1, the ability of AFAP1-AS1 to recruit EZH2 was remarkably attenuated. Knockdown of AFAP1-AS1 or EZH2 upregulated KLF2 expression in GC cells. Notably, knockdown of KLF2 partially reversed the effect of AFAP1-AS1 on GC cell performances.

CONCLUSIONS: LncRNA AFAP1-AS1 accelerates the proliferative and migratory abilities of GC cells by downregulating the expression of KLF2, thus promoting the progression of GC.

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