Clinical value and biological role of LINC00978 in non-small cell lung cancer
10.13602/j.cnki.jcls.2019.08.09
- VernacularTitle:LINC00978在非小细胞肺癌中的临床价值和生物学作用
- Author:
Yan HU
1
;
Xiaoge DING
2
;
Jianmei GU
3
;
Sinan HOU
1
;
Yanke CHEN
2
;
Xueyan ZANG
2
;
Jiayin ZHANG
2
;
Yu ZHANG
2
;
Meng SHAO
2
;
Zheying MAO
2
;
Hui QIAN
2
;
Wenrong XU
2
;
Xu ZHANG
2
Author Information
1. Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University; Department of Clinical Laboratory, Lianyungang Hospital of Traditional Chinese Medicine
2. Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University
3. Department of Clinical Laboratory, Nantong Tumor Hospital
- Publication Type:Journal Article
- Keywords:
long non-coding RNA;
non-small cell lung cancer;
LINC00978;
epithelial-mesenchymal transformation
- From:
Chinese Journal of Clinical Laboratory Science
2019;37(8):596-602
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC).
Methods:The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively.
Results:The expression levels of LINC00978 in the tissues ( t =2.465, P ＜0.05) and serum samples ( t =8.781, P ＜0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P ＜0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P ＜0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P ＜0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P ＜0.05). The overexpression of LINC00978 had the opposite effect.
Conclusion:LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.
