Knockdown of lncRNA IGF2BP2-AS1 inhibits proliferation and migration of oral squamous cell carcinoma cells via the Wnt/β-catenin pathway.

J Oral Pathol Med

Department of Clinical Laboratory, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250021, China.

Published: March 2022

Background: Long non-coding RNA IGF2BP2 antisense RNA1 (lncRNA IGF2BP2-AS1) has been used to predict the overall survival rate of lung squamous cell carcinoma. This research aims to investigate the effect of IGF2BP2-AS1 in oral squamous cell carcinoma (OSCC).

Methods: The TCGA database was applied to evaluate the level of IGF2BP2-AS1 and its correlation with the clinicopathological characteristics of OSCC. The levels of IGF2BP2-AS1 in 30 OSCC and 20 normal tissue samples were detected by RT-qPCR. The distributions of IGF2BP2-AS1 in two OSCC cell lines (ie, Cal27 and SCC9) were detected by FISH. Colony formation, flow cytometry, wound-healing, transwell, and Western blotting analyses were used for evaluating the effect of IGF2BP2-AS1 on OSCC progression.

Results: In comparison with the normal tissue samples, OSCC showed higher expression of IGF2BP2-AS1. High expression of IGF2BP2-AS1 was associated with poor survival in OSCC patients. Results of FISH showed that IGF2BP2-AS1 was mainly present in the cytoplasm. Further in vitro functional tests demonstrated that downregulation of IGF2BP2-AS1 in Cal27 and SCC9 cells significantly inhibited cell proliferation and migration, leading to cell-cycle arrest and cell apoptosis. Western blotting showed that expressions of β-catenin, Cyclin D1, Bcl-2, and MMP2 were downregulated, whereas Bax was upregulated following knockdown of IGF2BP2-AS1. The inhibitory effect of knockdown of IGF2BP2-AS1 on migration could be partially reversed by the Wnt/β-catenin pathway stimulator LiCl.

Conclusion: Our results suggest that knockdown of IGF2BP2-AS1 suppresses cell growth, migration and promotes apoptosis in OSCC cells, providing a new molecular target for OSCC.

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Source
http://dx.doi.org/10.1111/jop.13248DOI Listing

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