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Updated: Nov 23, 2025
Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Identifying the p65-Dependent Effect of Sulforaphene on Esophageal Squamous Cell Carcinoma Progression via
Sichong Han1, Zhe Wang1, Jining Liu1
1State Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing 100029, China.
Abstract:
Understanding the mechanism by which sulforaphene (SFE) affects esophageal squamous cell carcinoma (ESCC) contributes to the application of this isothiocyanate as a chemotherapeutic agent. Thus, we attempted to investigate SFE regulation of ESCC characteristics more deeply. We performed gene set enrichment analysis (GSEA) on microarray data of SFE-treated ESCC cells and found that differentially expressed genes are enriched in TNFα_Signaling_via_the_NFκB_Pathway. Coupled with the expression profile data from the GSE20347 and GSE75241 datasets, we narrowed the set to 8 genes, 4 of which (C-X-C motif chemokine ligand 10 (CXCL10), TNF alpha induced protein 3 (TNFAIP3), inhibin subunit beta A (INHBA), and plasminogen activator, urokinase (PLAU)) were verified as the targets of SFE. RNA-sequence (RNA-seq) data of 182 ESCC samples from The Cancer Genome Atlas (TCGA) were grouped into two phenotypes for GSEA according to the expression of CXCL10, TNFAIP3, INHBA, and PLAU. The enrichment results proved that they were all involved in the NFκB pathway. ChIP-seq analyses obtained from the Cistrome database indicated that NFκB-p65 is likely to control the transcription of CXCL10, TNFAIP3, INHBA, and PLAU, and considering TNFAIP3 and PLAU are the most significantly differentially expressed genes, we used chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR) to verify the regulation of p65 on their expression. The results demonstrated that SFE suppresses ESCC progression by down-regulating TNFAIP3 and PLAU expression in a p65-dependent manner.
Insights
Sulforaphene (SFE) suppresses esophageal squamous cell carcinoma (ESCC) progression by down-regulating TNFAIP3 and PLAU expression. This occurs in a p65-dependent manner, highlighting SFE
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Esophageal squamous cell carcinoma (ESCC) is a significant global health concern.
- Sulforaphene (SFE), an isothiocyanate, shows potential as a chemotherapeutic agent.
- Understanding SFE's mechanism in ESCC is crucial for its clinical application.
Purpose of the Study:
- To investigate the molecular mechanisms by which SFE regulates ESCC progression.
- To identify specific molecular targets of SFE in ESCC cells.
Main Methods:
- Gene Set Enrichment Analysis (GSEA) on microarray and RNA-seq data.
- Analysis of The Cancer Genome Atlas (TCGA) datasets (GSE20347, GSE75241).
- Chromatin Immunoprecipitation (ChIP-seq and ChIP-PCR) to assess transcription factor binding.
Main Results:
- SFE treatment enriched genes in the TNFα Signaling via the NFκB Pathway.
- Four key genes (CXCL10, TNFAIP3, INHBA, PLAU) were identified as SFE targets.
- NFκB-p65 was confirmed to regulate TNFAIP3 and PLAU transcription, mediating SFE's suppressive effect.
Conclusions:
- SFE suppresses ESCC progression through the NFκB pathway.
- SFE down-regulates TNFAIP3 and PLAU expression in a p65-dependent manner.
- These findings support SFE's potential as a targeted therapy for ESCC.
