Skip to content
DraconiticResearch
Search Sources API
203,203 studies31 sourcesUpdated 37 min ago
Peer-reviewedCC BY 4.0Frontiers in Immunology

Regulatory network remodeling and potential non-canonical associations of the transcription factor SP1 during inflammation-to-cancer transformation in esophageal squamous cell carcinoma

  • Bin Du1,2
  • Jie Zhang2
  • Huimin Liu2
  • Xiaoya Xing2
  • Xinyue Wang2
  • Pu Wang2
  1. 1Shanxi Key Laboratory of Aging Mechanism Research and Translational Applications, Changzhi Medical College
  2. 2School of Basic Medical Sciences, Changzhi Medical College
Read full textPDFDOICite

Abstract

Background: Esophageal squamous cell carcinoma (ESCC) is closely linked to chronic inflammation, but the transcriptional mechanisms connecting epithelial inflammatory remodeling with malignant transformation remain incompletely understood.

Methods: We integrated secondary analysis of published single-cell epithelial transition-state data, virtual SP1 perturbation, TCGA analyses, xCell immune infiltration analysis, TIDE-based exploratory immunotherapy prediction, Co-IP/MS, and a 4NQO-induced mouse model to investigate SP1-associated network remodeling during ESCC carcinogenesis.

Results: SP1 regulatory importance increased across pairwise epithelial state comparisons. In adjacent normal epithelial cells, virtual SP1 overexpression affected genes linked to inflammatory response, NF-κB-related signaling, epithelial stress remodeling, and proliferation. SP1 expression correlated with immune infiltration features and immune checkpoint gene expression, and TIDE analysis suggested an association with predicted immunotherapy-related features. SP1-binding partners were enriched in RNA metabolism, RNA splicing, and nuclear protein-complex annotations, suggesting potential non-canonical regulatory associations that require further experimental validation.

Conclusions: SP1 may represent a progressively enhanced transcriptional hub during inflammation-associated ESCC carcinogenesis, with state-dependent network remodeling spanning epithelial inflammatory stress, malignant transformation, and tumor immune features.

Related

  1. Tongxinluo is associated with neurovascular changes following rt-PA-treated ischemic stroke: associations with inflammation, vascular remodeling, and neural plasticity
    Meiling Xiao, Wei Ding, Xiaoqu Zuo +1
    Frontiers in NeurologyPeer-reviewedCC BY 4.0Full textEpidemiology & public healthCrossrefEurope PMCPMC
  2. Transcription Regulatory Sequences in Coronaviruses: Mechanistic Foundations for Antivirals and Vaccines.
    Jinjong Myoung
    Journal of microbiology and biotechnologyPeer-reviewedCC BYFull textInfectious diseaseEurope PMC
  3. Aberrant Transcription-Factor Expression and Regulatory microRNAs in Metastatic Breast Cancer
    Eman Hillal Althubaiti
    CellsPeer-reviewedCC BY 4.0OncologyCrossref
  4. SMARCA4 MUTATIONS PROMOTE CHEMOTHERAPY RESISTANCE IN T-ACUTE LYMPHOBLASTIC LEUKEMIA THROUGH ALTERED CHROMATIN REMODELING AT AP1-ASSOCIATED REGULATORY REGIONS
    V. Garcia-Hernandez, M. Maqueda, G. Faccincani +10
    bioRxivPreprintAll rights reservedFull textOncologybioRxiv
  5. Chronic Inflammation, Fibrotic Remodeling, and Regenerative Failure in Duchenne Muscular Dystrophy: Mechanisms and Therapeutic Opportunities
    Jie Shi, Jiao Yang
    BiomedicinesPeer-reviewedCC BYFull textGeneral medicineEurope PMC

Cite

BibTeXRIS
BibTeX
@article{du2026regulatory,
  title = {{Regulatory network remodeling and potential non-canonical associations of the transcription factor SP1 during inflammation-to-cancer transformation in esophageal squamous cell carcinoma}},
  author = {Bin Du and Jie Zhang and Huimin Liu and Xiaoya Xing and Xinyue Wang and Pu Wang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1919461},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1919461/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Regulatory network remodeling and potential non-canonical associations of the transcription factor SP1 during inflammation-to-cancer transformation in esophageal squamous cell carcinoma
AU  - Bin Du
AU  - Jie Zhang
AU  - Huimin Liu
AU  - Xiaoya Xing
AU  - Xinyue Wang
AU  - Pu Wang
PY  - 2026
DA  - 2026/10/16
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1919461
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1919461/full
AB  - Background: Esophageal squamous cell carcinoma (ESCC) is closely linked to chronic inflammation, but the transcriptional mechanisms connecting epithelial inflammatory remodeling with malignant transformation remain incompletely understood.  Methods: We integrated secondary analysis of published single-cell epithelial transition-state data, virtual SP1 perturbation, TCGA analyses, xCell immune infiltration analysis, TIDE-based exploratory immunotherapy prediction, Co-IP/MS, and a 4NQO-induced mouse model to investigate SP1-associated network remodeling during ESCC carcinogenesis.  Results: SP1 regulatory importance increased across pairwise epithelial state comparisons. In adjacent normal epithelial cells, virtual SP1 overexpression affected genes linked to inflammatory response, NF-κB-related signaling, epithelial stress remodeling, and proliferation. SP1 expression correlated with immune infiltration features and immune checkpoint gene expression, and TIDE analysis suggested an association with predicted immunotherapy-related features. SP1-binding partners were enriched in RNA metabolism, RNA splicing, and nuclear protein-complex annotations, suggesting potential non-canonical regulatory associations that require further experimental validation.  Conclusions: SP1 may represent a progressively enhanced transcriptional hub during inflammation-associated ESCC carcinogenesis, with state-dependent network remodeling spanning epithelial inflammatory stress, malignant transformation, and tumor immune features.
SN  - 1664-3224
ER  -