Long noncoding RNA expression profile in HLE B-3 cells during TGF-β2-induced epithelial-mesenchymal transition

17Citations
Citations of this article
8Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: Recent evidence has shown that long noncoding RNAs (lncRNAs) are involved in the process of epithelial-mesenchymal transition (EMT). However, little research has focused on the expression profile of lncRNAs during EMT in human lens epithelial cells (LECs) and their functions have not yet been described. Methods: Dysregulated lncRNAs and mRNAs in normal human lens epithelial B-3(HLE B-3) cells and during transforming growth factor β2(TGF-β2)-induced EMT were analyzed via lncRNA microarray. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway analyses of differentially expressed mRNAs were performed to identify their functions and pathologic pathways. Six candidate lncRNAs were validated via quantitative real-time reverse transcription polymerase chain reaction(qRT-PCR) to confirm the microarray data. Results: A total of 775 lncRNAs (325 up-regulated and 450 down-regulated) and 935 mRNAs (329 up-regulated and 606 down-regulated) were differentially expressed in HLE B-3 cells during TGF-β2-induced EMT compared to normal HLE B-3 cells. GO and KEGG Pathway analyses indicated the functions of differentially expressed mRNAs in the TGF-β2-induced EMT in HLE B-3 cells. qRT-PCR confirmed the trends indicated in microarray analysis for all 6 candidate lncRNAs. Conclusion: Our study lays the foundation for future research in lncRNAs related to EMT in HLE B-3 cells and could provide new avenues for the prevention and treatment of posterior capsule opacification (PCO).

Cite

CITATION STYLE

APA

Zhang, B., Chen, Y., Qiu, M., & Ding, Z. (2017). Long noncoding RNA expression profile in HLE B-3 cells during TGF-β2-induced epithelial-mesenchymal transition. BMC Ophthalmology, 17(1). https://doi.org/10.1186/s12886-017-0461-z

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free