MNAT1 expression in non-small cell lung cancer and its biological cellular impact
10.3760/cma.j.issn.0529-5807.2019.08.008
- VernacularTitle: MNAT1在非小细胞肺癌的表达及对其细胞生物学行为的影响
- Author:
Ya CHEN
1
;
Jiexia GUAN
;
Hong SHEN
Author Information
1. Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
- Publication Type:Journal Article
- Keywords:
Lung neoplasms;
Cyclin-dependent kinases;
Cell cycle;
Cell proliferation;
Gene silencing
- From:
Chinese Journal of Pathology
2019;48(8):626-632
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression and significance of MNAT1 in non-small cell lung cancer (NSCLC) and to explore the biological impact of MNAT1 expression in lung cancer cells at the cellular level and related signaling pathway.
Methods:Forty-eight cases of NSCLC tissues and paired normal tissues was collected at Nanfang Hospital, Southern Medical University from 2015 to 2017. The expression level of MNAT1 was detected by immunohistochemistry, and the relationship between MNAT1 and clinicopathological features was analyzed. The expression of MNAT1 was detected in lung cancer cells, MNAT1 level was analyzed after knocking down in A549 and H322 cells by siRNA; Plasmid vector of overexpressing MNAT1 was constructed, followed by transfecting H1299 cells and observing proliferation and migration at the cellular level. Flow cytometry was used to analyze the effect of the expression of MNAT1 on cell cycle, and Western blot was used to explore the possible molecular mechanism of MNAT1 on cell proliferation and cell cycle.
Results:Immunohistochemistry showed that the expression score of MNAT1 was (4.07±3.55) in normal lung tissue and (7.33±4.09) in NSCLC tissue (P<0.01), and correlated with lymph node metastasis. At the cellular level, MNAT1 promoted cell proliferation(P<0.05), migration(P<0.05) and cell cycle progression(P<0.01).
Conclusions:MNAT1 may be involved in the development of non-small cell lung cancer.MNAT1 affects cell cycle and proliferation through the Akt/p21 pathway.
