X-Z Hao1, K Yang. 1. Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.hzh2004511@Sina.com.
Abstract
OBJECTIVE: To uncover the biological role of long non-coding RNA (lncRNA) MAGI2-AS3 in the progression of non-small cell lung carcinoma (NSCLC) and its molecular mechanism. PATIENTS AND METHODS: LncRNA MAGI2-AS3 level in NSCLC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Chi-square test was conducted to analyze the correlation between MAGI2-AS3 level and pathological characteristics of NSCLC patients. Survival analysis was performed in NSCLC patients with high expression or low expression of MAGI2-AS3. In vitro influences of MAGI2-AS3 on viability and invasive ability of A549 and PC9 cells were evaluated. MicroRNA-23a-3p (miRNA-23a-3p), the target gene of MAGI2-AS3 was determined through the dual-luciferase reporter gene assay. In a similar way, the target gene of miRNA-23a-3p was identified. Finally, the regulatory effect of MAGI2-AS3/miRNA-23a-3p/PTEN (gene of phosphate and tension homology deleted on chromosome ten) axis on cellular behaviors of NSCLC cells was assessed. RESULTS: LncRNA MAGI2-AS3 was downregulated in NSCLC tissues and cell lines. Its level was closely related to tumor size, Tumor Node Metastasis (TNM) stage and distant metastasis of NSCLC patients. The worse prognosis was identified in NSCLC patients with low expression of MAGI2-AS3 relative to those with a high expression. Overexpression of MAGI2-AS3 markedly attenuated viability and invasive ability of A549 and PC9 cells. MiRNA-23a-3p was verified to be the target gene of MAGI2-AS3, and furthermore, PTEN was the target of miRNA-23a-3p. Overexpression of miRNA-23a-3p could reverse the inhibited viability and invasion in NSCLC cells overexpressing MAGI2-AS3. CONCLUSIONS: MAGI2-AS3 is downregulated in NSCLC. Overexpression of MAGI2-AS3 suppresses the proliferative and invasive abilities of NSCLC via miRNA-23a-3p/PTEN axis.
OBJECTIVE: To uncover the biological role of long non-coding RNA (lncRNA) MAGI2-AS3 in the progression of non-small cell lung carcinoma (NSCLC) and its molecular mechanism. PATIENTS AND METHODS: LncRNA MAGI2-AS3 level in NSCLC tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Chi-square test was conducted to analyze the correlation between MAGI2-AS3 level and pathological characteristics of NSCLCpatients. Survival analysis was performed in NSCLCpatients with high expression or low expression of MAGI2-AS3. In vitro influences of MAGI2-AS3 on viability and invasive ability of A549 and PC9 cells were evaluated. MicroRNA-23a-3p (miRNA-23a-3p), the target gene of MAGI2-AS3 was determined through the dual-luciferase reporter gene assay. In a similar way, the target gene of miRNA-23a-3p was identified. Finally, the regulatory effect of MAGI2-AS3/miRNA-23a-3p/PTEN (gene of phosphate and tension homology deleted on chromosome ten) axis on cellular behaviors of NSCLC cells was assessed. RESULTS: LncRNA MAGI2-AS3 was downregulated in NSCLC tissues and cell lines. Its level was closely related to tumor size, Tumor Node Metastasis (TNM) stage and distant metastasis of NSCLCpatients. The worse prognosis was identified in NSCLCpatients with low expression of MAGI2-AS3 relative to those with a high expression. Overexpression of MAGI2-AS3 markedly attenuated viability and invasive ability of A549 and PC9 cells. MiRNA-23a-3p was verified to be the target gene of MAGI2-AS3, and furthermore, PTEN was the target of miRNA-23a-3p. Overexpression of miRNA-23a-3p could reverse the inhibited viability and invasion in NSCLC cells overexpressing MAGI2-AS3. CONCLUSIONS:MAGI2-AS3 is downregulated in NSCLC. Overexpression of MAGI2-AS3 suppresses the proliferative and invasive abilities of NSCLC via miRNA-23a-3p/PTEN axis.