Expression and biological role of LncSox4 in non-small cell lung cancer
10.13602/j.cnki.jcls.2019.10.03
- VernacularTitle:LncSox4在非小细胞肺癌中的表达及生物学作用
- Author:
Sinan HOU
1
,
2
;
Yanke CHEN
1
;
Jianmei GU
3
;
Xiaoge DING
1
;
Jiayin ZHANG
1
;
Hui QIAN
1
;
Wenrong XU
1
;
Xu ZHANG
1
Author Information
1. Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University
2. Department of Clinical Laboratory, Lianyungang Traditional Chinese Medicine Hospital
3. Department of Clinical Laboratory, Nantong Tumor Hospital
- Publication Type:Journal Article
- Keywords:
long non-coding RNA;
non-small cell lung cancer;
LncSox4;
epithelial-mesenchymal transition
- From:
Chinese Journal of Clinical Laboratory Science
2019;37(10):731-736
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To determine the changed expression levels, biological roles and underlying mechanism of LncSox4 in non-small cell lung cancer (NSCLC), providing novel biomarkers for NSCLC diagnosis and therapy.
Methods:QRT-PCR was used to detect the expression of LncSox4 in the tumor tissues of NSCLC patients. Colony formation, cell growth curve, Transwell migration and invasion assays were used to determine the effects of LncSox4 knockdown on A549 cell function, respectively. Flow cytometry was used to determine the effects of LncSox4 on the progression of A549 cell cycle. QRT-PCR and western blot were used to explore the expressions of genes and proteins in epithelial-mesenchymal transition (EMT).
Results:The expression of LncSox4 was upregulated significantly in carcinoma tissues of NSCLC compared to the para-carcinoma tissues (t=7.109，P＜0.01). The growth rate of A549 cells slowed down in LncSox4 knockdown group and the number of formed cell colonies was less than that in control group(P＜0.01). LncSox4 knockdown reduced the migration and invasion abilities of A549 cells (P＜0.01) and induced cell cycle arrest at G1 phase(P＜0.01). LncSox4 knockdown downregulated the protein expressions of Cyclin D1, c-Myc, N-cadherin, and Vimentin, while upregulated the expression of E-cadherin in A549 cells. LncSox4 knockdown also decreased the expressions of EMT-related transcription factors including snail, slug and twist.
Conclusion:The high expression of LncSox4 in NSCLC may promote malignant progression of NSCLC by enhancing cell proliferation, migration and invasion, suggesting that it should be a promising target for diagnosis and therapy of NSCLC.
