Digestive Diseases and Sciences

, Volume 62, Issue 8, pp 2004–2010 | Cite as

Long Noncoding RNA AFAP1-AS1 Promotes Cell Proliferation and Apoptosis of Gastric Cancer Cells via PTEN/p-AKT Pathway

  • Jun-qiang Guo
  • Shi-jie Li
  • Guo-xiao Guo
Original Article



Long noncoding RNA (lncRNA) plays critical roles in both tumor-suppressive and oncogenic pathways in the pathological development and prognosis of cancers.


This study aimed to explore the expression of lncRNA AFAP1-AS1 and its function in gastric cancer (GC).


The expression of AFAP1-AS1 was detected in GC tissues and GC cells by quantitative real-time reverse-transcription PCR. A small interfering RNA (siRNA) that targeted AFAP1-AS1 was transfected into cells to inhibit the expression of AFAP1-AS1. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and colony formation assay were performed to examine the cell proliferation of SGC7901 cell transfected with si-AFAP1-AS1. Cell apoptosis was detected by flow cytometry. The protein level of cleaved PARP, Caspase 3, Caspase 9, Caspase 8, Bcl-2, Bax, p-AKT, total-AKT, and PTEN were detected by Western blot.


AFAP1-AS1 was up-regulated in GC tissues and GC cells. AFAP1-AS1 knockdown suppressed cell viability of SGC7901 transfected with si-AFAP1-AS1. The number of apoptotic SGC7901 cell transfected with si-AFAP1-AS1 was increased by 3.4-fold comparing to that of control. The protein level of cleaved PARP, Caspase 3, and Caspase 9 were increased in SGC7901 transfected with si-AFAP1-AS1, as well as the expression of Bax. The protein level of Bcl-2 was decreased. AFAP1-AS1 knockdown decreased the protein level of p-AKT and increased the expression of PTEN in SGC7901 cells.


AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.


AFAP1-AS1 Gastric cancer Proliferation Apoptosis PTEN p-AKT 


Compliance with ethical standards

Conflict of interest

The authors have no actual or potential conflicts of interest to declare.


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Copyright information

© Springer Science+Business Media New York 2017

Authors and Affiliations

  1. 1.Department of Institute of Traumatic Surgery, Huaihe HospitalHenan UniversityKaifengChina
  2. 2.Department of General Surgery, Huaihe HospitalHenan UniversityKaifengChina

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