Upregulation of LINC02154 promotes esophageal cancer progression by enhancing cell cycling and epithelial-mesenchymal transition

TL;DR

This study identifies LINC02154 as a long noncoding RNA that promotes esophageal cancer progression by enhancing cell growth and cancer spread.

Contribution

The study reveals LINC02154 as a novel oncogenic lncRNA in esophageal cancer and identifies its role in cell cycling, EMT, and chemoresistance.

Findings

LINC02154 is significantly upregulated in primary esophageal cancer tumors and correlates with advanced T stages.

Knockdown of LINC02154 reduces cell proliferation and migration in ESCA cell lines.

LINC02154 promotes EMT and chemoresistance by suppressing miR-200b and interacts with desmosome-related proteins.

Abstract

Long noncoding RNAs (lncRNAs) play crucial roles in the progression of human malignancies; however, their involvement in esophageal cancer (ESCA) remains incompletely understood. In this study, we screened for lncRNAs upregulated in ESCA and identified 12 lncRNAs significantly upregulated in primary ESCA tumors. Among those, elevated LINC02154 expression correlated positively with advanced T stages. LINC02154 knockdown in ESCA cell lines suppressed cell proliferation and migration, while ectopic expression of LINC02154 enhanced colony formation. Depletion of LINC02154 suppressed genes involved in various oncogenic processes, including cell cycling, epithelial-mesenchymal transition (EMT), and metabolism. We also found that LINC02154 promotes EMT and enhances chemoresistance, at least in part, through suppression of miR-200b. Finally, RNA-pulldown and mass spectrometry analysis revealed that LINC02154 interacts with proteins involved in the cornified envelope or desmosome. These findings suggest that LINC02154 exerts oncogenic effects through modulation of multiple oncogenic signaling pathways in ESCA and that LINC02154 is a potential therapeutic target.

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