SP1-activated LINC01638 promotes proliferation and migration of gastric cancer cells by regulating epithelial-mesenchymal transition

X.-J. Wu, Y.-H. Yang, K.-X. Wang

Department of Pathology, Weihaiwei People’s Hospital, Weihai, China. 574244171@qq.com

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• Oncology

OBJECTIVE: The aim of this study was to detect the expression of long intergenic non-protein coding ribonucleic acid 01638 (LINC01638) in gastric cancer (GC), and to explore its role and molecular mechanism in regulating the proliferation and metastasis of GC cells.

PATIENTS AND METHODS: The relative expression level of LINC01638 in 50 cases of GC tissues and paracancerous tissues and GC cells was determined using quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). After interference with the expression of LINC01638, the interference efficiency was detected via qRT-PCR, and the changes in GC cell proliferation ability, cell cycle distribution, and migration and invasion abilities were examined using colony formation assay, flow cytometry, and transwell assay, respectively. The possible transcription factors binding to the promoter region of LINC01638 were predicted using bioinformatics methods. After interference with specificity protein 1 (SP1), qRT-PCR was performed to detect the interference efficiency and the change in LINC01638 expression. Besides, the changes in the molecular markers for epithelial-mesenchymal transition (EMT) were detected using Western blotting assay after interfering with LINC01638 expression and using Western blotting after interfering with SP1.

RESULTS: The expression of LINC01638 was upregulated in 40 cases of GC tissues, and its expression level in GC cells was higher than that in normal gastric mucosal cells. After interfering with the expression of LINC01638, the colony formation assay results showed that the proliferation of GC cells was suppressed, it was found through flow cytometry that the cell cycle was arrested in G1/G0 phase, and transwell assay results manifested that the cell migration and invasion abilities declined. According to the bioinformatics and qRT-PCR results, the transcription factor SP1 contributed to the expression of LINC01638, and the expressions of molecular markers in the EMT signaling pathway were changed after interfering with LINC0168 and SP1.

CONCLUSIONS: In this study, it was verified through the in vitro experiments that LINC01638 promotes the migration and invasion of GC by regulating EMT.

 

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