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Updated: Feb 13, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Identification of key genes and long non‑coding RNAs in celecoxib‑treated lung squamous cell carcinoma cell line by
Gang Li1, Xuehai Wang1, Qingsong Luo1
1Department of Thoracic Surgery, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.
Abstract:
Celecoxib is an inhibitor of cyclooxygenase-2, a gene that is often aberrantly expressed in the lung squamous cell carcinoma (LSQCC). The present study aims to provide novel insight into chemoprevention by celecoxib treatment. The human LSQCC cell line SK‑MES‑1 was treated with or without celecoxib and RNA‑sequencing (RNA‑seq) was performed on the Illumina HiSeq 2000 platform. Expression levels of genes or long non‑coding RNAs (lncRNAs) were calculated by Cufflinks software. Subsequently, differentially expressed genes (DEGs) and differentially expressed lncRNAs (DE‑LNRs) between the two groups were selected using the limma package and LNCipedia 3.0, respectively; followed by co‑expression analysis based on their expression correlation coefficient (CC). Enrichment analysis for the DEGs and co‑expressed DE‑LNRs were performed. Protein‑protein interaction (PPI) network analysis for DEGs was performed using STRING database. A set of 317 DEGs and 25 DE‑LNRs were identified between celecoxib‑treated and non‑treated cell lines. A total of 12 pathways were enriched by the DEGs, including 'protein processing in endoplasmic reticulum' for activating transcription factor 4 (ATF4), 'mammalian target of rapamycin (mTOR) signaling pathway' for vascular endothelial growth factor A (VEGFA) and 'ECM‑receptor interaction' for fibronectin 1 (FN1). Genes such as VEGFA, ATF4 and FN1 were highlighted in the PPI network. VEGFA was linked with lnc‑AP000769.1‑2:10 (CC= ‑0.99227), whereas ATF4 and FN1 were closely correlated with lnc‑HFE2‑2:1 (CC=0.996159 and ‑0.98714, respectively). lncRNAs were also enriched in pathways such as 'mTOR signaling pathway' for lnc‑HFE2‑2:1. Several important molecules were identified in celecoxib‑treated LSQCC cell lines, such as VEGFA, ATF4, FN1, lnc‑AP000769.1‑2:10 and lnc‑HFE2‑2:1, which may enhance the anti‑cancer effects of celecoxib on LSQCC.
Insights
Celecoxib treatment in lung squamous cell carcinoma (LSQCC) revealed significant gene and long non-coding RNA expression changes. Key molecules like VEGFA, ATF4, and FN1 were identified, potentially enhancing celecoxib
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Lung squamous cell carcinoma (LSQCC) exhibits aberrant cyclooxygenase-2 (COX-2) expression.
- Celecoxib, a COX-2 inhibitor, is investigated for its chemopreventive potential in LSQCC.
- Understanding molecular targets is crucial for developing effective LSQCC therapies.
Purpose of the Study:
- To investigate the molecular mechanisms of celecoxib chemoprevention in LSQCC.
- To identify differentially expressed genes (DEGs) and long non-coding RNAs (lncRNAs) upon celecoxib treatment.
- To explore the functional roles of identified molecules in LSQCC.
Main Methods:
- RNA-sequencing (RNA-seq) was performed on the human LSQCC cell line SK-MES-1.
- Differential expression analysis for genes and lncRNAs was conducted using limma and LNCipedia.
- Co-expression, enrichment, and protein-protein interaction (PPI) network analyses were employed.
Main Results:
- 317 DEGs and 25 differentially expressed lncRNAs (DE-LNRs) were identified.
- Enriched pathways included 'protein processing in endoplasmic reticulum' (ATF4), 'mTOR signaling pathway' (VEGFA), and 'ECM-receptor interaction' (FN1).
- Key molecules VEGFA, ATF4, FN1, lnc-AP000769.1-2:10, and lnc-HFE2-2:1 were highlighted and correlated with specific pathways.
Conclusions:
- Celecoxib treatment significantly alters gene and lncRNA expression in LSQCC.
- Identified molecules like VEGFA, ATF4, and FN1, along with specific lncRNAs, may mediate celecoxib's anti-cancer effects.
- These findings provide novel insights into celecoxib's chemopreventive mechanisms in LSQCC.
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