Jun-Qiang Guo1, Shi-Jie Li1, Guo-Xiao Guo2. 1. Department of Institute of Traumatic Surgery, Huaihe Hospital, Henan University, Kaifeng, 475000, China. 2. Department of General Surgery, Huaihe Hospital, Henan University, No. 1 Baobei Rd., Kaifeng, 475000, Henan, China. guogxiao@126.com.
Abstract
BACKGROUND: Long noncoding RNA (lncRNA) plays critical roles in both tumor-suppressive and oncogenic pathways in the pathological development and prognosis of cancers. AIMS: This study aimed to explore the expression of lncRNA AFAP1-AS1 and its function in gastric cancer (GC). METHODS: 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. RESULTS: 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. CONCLUSIONS: AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.
BACKGROUND: Long noncoding RNA (lncRNA) plays critical roles in both tumor-suppressive and oncogenic pathways in the pathological development and prognosis of cancers. AIMS: This study aimed to explore the expression of lncRNA AFAP1-AS1 and its function in gastric cancer (GC). METHODS: 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. RESULTS: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. CONCLUSIONS:AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway.
Authors: J A McCubrey; L S Steelman; S L Abrams; F E Bertrand; D E Ludwig; J Bäsecke; M Libra; F Stivala; M Milella; A Tafuri; P Lunghi; A Bonati; A M Martelli Journal: Leukemia Date: 2008-03-13 Impact factor: 11.528
Authors: M Katie Conley-LaComb; Allen Saliganan; Pridvi Kandagatla; Yong Q Chen; Michael L Cher; Sreenivasa R Chinni Journal: Mol Cancer Date: 2013-07-31 Impact factor: 27.401