Feng Li1, Qing Hu1, Zhonghao Pang1, Xiuquan Xu2. 1. Department of Thoracic Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China. 2. Pharmacy School of Jiangsu University, Zhenjiang, China.
Abstract
Background: MAGI2-AS3 has been reported to be a tumor suppressor in breast cancer and bladder cancer. This study analyzed the role of MAGI2-AS3 in non-small cell lung cancer (NSCLC). Results: The authors found that MAGI2-AS3 and suppressor of cytokine signaling 1 (SOCS-1) were both downregulated in NSCLC. MAGI2-AS3 and SOCS-1 were significantly and positively correlated in NSCLC tumor tissues. During follow-up, low levels of MAGI2-AS3 and SOCS-1 were found to be significantly correlated with patients' poor survival. In NSCLC cells, MAGI2-AS3 overexpression mediated the upregulated, while miR-155 expression mediated the downregulated SOCS-1 overexpression. RNA binding analysis showed that MAGI2-AS3 may be a sponge of miR-155. Cell proliferation revealed decreased cell proliferation rate of NSCLC cells after MAGI2-AS3 and SOCS-1 overexpression. MiR-155 played an opposite role and reduced the effects of MAGI2-AS3 overexpression. Conclusion: Therefore, MAGI2-AS3 upregulates cytokine signaling 1 by sponging miR-155 to inhibit NSCLC cell proliferation.
Background: MAGI2-AS3 has been reported to be a tumor suppressor in breast cancer and bladder cancer. This study analyzed the role of MAGI2-AS3 in non-small cell lung cancer (NSCLC). Results: The authors found that MAGI2-AS3 and suppressor of cytokine signaling 1 (SOCS-1) were both downregulated in NSCLC. MAGI2-AS3 and SOCS-1 were significantly and positively correlated in NSCLC tumor tissues. During follow-up, low levels of MAGI2-AS3 and SOCS-1 were found to be significantly correlated with patients' poor survival. In NSCLC cells, MAGI2-AS3 overexpression mediated the upregulated, while miR-155 expression mediated the downregulated SOCS-1 overexpression. RNA binding analysis showed that MAGI2-AS3 may be a sponge of miR-155. Cell proliferation revealed decreased cell proliferation rate of NSCLC cells after MAGI2-AS3 and SOCS-1 overexpression. MiR-155 played an opposite role and reduced the effects of MAGI2-AS3 overexpression. Conclusion: Therefore, MAGI2-AS3 upregulates cytokine signaling 1 by sponging miR-155 to inhibit NSCLC cell proliferation.
Entities:
Keywords:
MAGI2-AS; SOCS-1; miR-155; non-small cell lung cancer