Negin Raei1, Reza Safaralizadeh2, Mohammadali Hosseinpourfeizi1, Saeid Latifi-Navid3, Abbas Yazdanbod4. 1. Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, 5166616471, Tabriz, Iran. 2. Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, 5166616471, Tabriz, Iran. safaralizadeh@tabrizu.ac.ir. 3. Department of Biology, Faculty of Sciences, University of Mohaghegh Ardabili, Ardabil, Iran. 4. Digestive Disease Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.
Abstract
BACKGROUND: Gastric cancer (GC) is a major malignancy that threatens people's lives worldwide. Long noncoding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) is known to be a potential oncogene in many cancers and may promote cell migration and metastasis, and decrease apoptosis rate. MATERIAL AND METHODS: NORAD expression was measured in 70 pairs of GC tissues and their adjacent normal tissues (ANTs) by quantitative real-time polymerase chain reaction. Si-NORAD gene knockdown study and cellular assays were conducted to assess the correlation between NORAD expression and cell viability, apoptosis, migration, and metastasis. RESULTS: NORAD was significantly overexpressed in GC tissues compared to ANTs (P value < 0.0001). The receiver operating characteristic curve indicated the AUC of 0.721 with the sensitivity and specificity of 78.57 and 61.43, respectively (P value < 0.0001). NORAD downregulation leads to decreased cell viability (P value < 0.001) and migration (P value < 0.01), increased apoptosis rate (P value < 0.0001), and increased protein level for PTEN, E-cadherin, and Bax, but decreased protein level for Bcl-2. CONCLUSION: Generally, NORAD may serve as a potential diagnostic biomarker in GC.
BACKGROUND: Gastric cancer (GC) is a major malignancy that threatens people's lives worldwide. Long noncoding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) is known to be a potential oncogene in many cancers and may promote cell migration and metastasis, and decrease apoptosis rate. MATERIAL AND METHODS: NORAD expression was measured in 70 pairs of GC tissues and their adjacent normal tissues (ANTs) by quantitative real-time polymerase chain reaction. Si-NORAD gene knockdown study and cellular assays were conducted to assess the correlation between NORAD expression and cell viability, apoptosis, migration, and metastasis. RESULTS: NORAD was significantly overexpressed in GC tissues compared to ANTs (P value < 0.0001). The receiver operating characteristic curve indicated the AUC of 0.721 with the sensitivity and specificity of 78.57 and 61.43, respectively (P value < 0.0001). NORAD downregulation leads to decreased cell viability (P value < 0.001) and migration (P value < 0.01), increased apoptosis rate (P value < 0.0001), and increased protein level for PTEN, E-cadherin, and Bax, but decreased protein level for Bcl-2. CONCLUSION: Generally, NORAD may serve as a potential diagnostic biomarker in GC.