AFAP1-AS1 is upregulated and promotes esophageal squamous cell carcinoma cell proliferation and inhibits cell apoptosis.
Hong-Lei LuoMing-de HuangJia-Ni GuoRui-Hua FanXiao-Tian XiaJing-Dong HeXiao-Fei ChenPublished in: Cancer medicine (2016)
Recent findings indicate that long noncoding RNAs (lncRNAs) were dysregulated in many kinds of tumors including esophageal squamous cell carcinoma (ESCC). LncRNA AFAP1-AS1 was found to be upregulated in hepatocellular carcinoma (HCC), lung cancer, colorectal cancer, esophageal adenocarcinoma (EAC), pancreatic ductal adenocarcinoma, and nasopharyngeal carcinoma, while its clinical value and potential function in ESCC are still unknown. Expression of AFAP1-AS1 was measured in 65 ESCC tissues and corresponding noncancerous tissues by quantitative real-time polymerase chain reaction, which revealed that AFAP1-AS1 expression was markedly elevated in ESCC tissues and significantly associated with advanced TNM stage (P = 0.004) and larger tumor size (P = 0.040). Moreover, by knocking down AFAP1-AS1 expression in ESCC cells, the proliferation and colony-forming ability were inhibited and cell apoptosis was induced. Our data indicated the first time that AFAP1-AS1, a novel oncogene, was remarkably upregulated and played a critical role in the progression of ESCC.
Keyphrases
- cell proliferation
- poor prognosis
- gene expression
- long non coding rna
- squamous cell carcinoma
- binding protein
- induced apoptosis
- signaling pathway
- cell cycle arrest
- radiation therapy
- cell death
- machine learning
- pi k akt
- risk assessment
- endothelial cells
- high glucose
- electronic health record
- big data
- mass spectrometry
- endoplasmic reticulum stress
- deep learning