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Archive > Volume 28 Issue 8 > 2021,28(8):775-782. DOI:10.3872/j.issn.1007-385X.2021.08.002 Prev Next
Basic Research
Expression of lncRNA LOC440173 in non-small cell lung cancer tissues and its influence on the maligant biological behaviors of cancer cells
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Abstract:
Objective: To detect the expression of lncRNA LOC440173 in NSCLC tissues and cells and to explore its influence on the maligant biological behavior of cancer cells. Methods: The cancer and para-cancerous tissues removed from 72 patients with NSCLC who were surgically during 2014 to 2017 in the biological specimen library of the Fourth Hospital of Hebei Medical University were selected. qPCR method was applied to detect the expression of LOC440173 in NSCLC tissues and the corresponding para-cancerous tissues as well as in six NSCLC cell lines (H520, H358, A549, HCC827, H1703 and H1299). The vectors used for LOC440173 knockdown or overexpression were constructed and transfected into H520 and H1703 cells, respectively. The effects of LOC440173 knockdown or overexpression on proliferation, migration, and invasion of lung cancer cells were examined by MTS, Clone formation, Transwell migration and invasion assays, respectively. qPCR method was used to detect the regulatory effect of LOC440173 on mRNA expression of EMT-related markers (E-cadherin, N-cadherin, and vimentin), WB method was employed to observe the protein expression of E-cadherin and N-cadherin. Results: The expression of LOC440173 in NSCLC tissues was significantly higher than that in corresponding para-cancerous tissues (P<0.01), and was correlated with lymph node metastasis, histological grade, TNM stage, and tumor size (P<0.05 or P<0.01). LOC440173 gene knockdown could inhibit the in vitro proliferation, invasion and migration of H520 cells (P<0.05 or P<0.01). Overexpression of LOC440173 gene significantly promoted the in vitro proliferation, migration, and invasion of H1703 cells (P<0.05 or P<0.01). At the transcriptional level, knockdown of LOC440173 was found to promote the expression level of E-cadherin and inhibit the expression level of N-cadherin and vimentin (P<0.05 or P<0.01), while overexpression of LOC440173 displayed the opposite results (P<0.05 or P<0.01). At the post-transcriptional level, LOC440173 negatively regulated protein expression of E-cadherin and positively modulated protein expression of N-cadherin (P<0.05). Conclusion: The abnormal high expression of LOC440173 may be related to the occurrence and development of NSCLC. LOC440173 can significantly improve the in vitro proliferation, migration and invasion of NSCLC cells, and the mechanism may be related to the regulation of EMT-related genes.
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Project Supported:
Project supported by the National Natural Science Foundation of China (No.81572441), and the Key Project of Medical Science Research of Hebei Province (No.20201050)
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