ΔNp63α‑mediated regulation of tumor‑associated genes and pathways in hepatocellular carcinoma progression.
- 1Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai Institute of Translational Medicine, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai, Guangdong 519000, P.R. China.
- 2Department of Pharmacy, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan, Shandong 250014, P.R. China.
Abstract
ΔNp63α is key in cellular development and epithelial tumors; however, its role in hepatocellular carcinoma (HCC) remains unclear. In the present study, the oncogenic role and molecular functions of ΔNp63α in HCC were investigated. Analysis of The Cancer Genome Atlas revealed an association between p63 expression and patient survival. ΔNp63α overexpression in SNU387 cells notably enhanced cell proliferation and migration, supporting its role in promoting aggressive HCC phenotypes. Transcriptome analysis revealed extensive ΔNp63α‑associated transcriptional changes, with differentially expressed genes enriched in tumor‑associated processes, including 'Wnt signaling pathway', 'Notch signaling pathway', 'cell adhesion molecules' and 'extracellular matrix organization'. Chromatin immunoprecipitation sequencing revealed widespread ΔNp63α binding in promoter‑proximal and ‑distal regulatory regions, suggesting potential involvement in transcriptional regulation through both proximal and distal genomic elements. ΔNp63α upregulation was also associated with increased CCCTC‑binding factor (CTCF) occupancy near the promoters of tumor‑associated genes and these gained CTCF sites were enriched for p63 motifs. Collectively, the present findings identified ΔNp63α as an oncogenic regulator of HCC and suggest that it may regulate tumor‑associated gene programs through coordinated proximal and distal chromatin regulatory mechanisms.
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BibTeX
@article{lin2026δnp63αmediated,
title = {{ΔNp63α‑mediated regulation of tumor‑associated genes and pathways in hepatocellular carcinoma progression.}},
author = {Xiaowen Lin and Anghui Peng and Min Zhang and Xinyang Yu},
journal = {Molecular medicine reports},
year = {2026},
month = oct,
doi = {10.3892/mmr.2026.14040},
url = {https://europepmc.org/article/MED/42885287},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - ΔNp63α‑mediated regulation of tumor‑associated genes and pathways in hepatocellular carcinoma progression.
AU - Xiaowen Lin
AU - Anghui Peng
AU - Min Zhang
AU - Xinyang Yu
PY - 2026
DA - 2026/10/16
JO - Molecular medicine reports
DO - 10.3892/mmr.2026.14040
UR - https://europepmc.org/article/MED/42885287
AB - ΔNp63α is key in cellular development and epithelial tumors; however, its role in hepatocellular carcinoma (HCC) remains unclear. In the present study, the oncogenic role and molecular functions of ΔNp63α in HCC were investigated. Analysis of The Cancer Genome Atlas revealed an association between p63 expression and patient survival. ΔNp63α overexpression in SNU387 cells notably enhanced cell proliferation and migration, supporting its role in promoting aggressive HCC phenotypes. Transcriptome analysis revealed extensive ΔNp63α‑associated transcriptional changes, with differentially expressed genes enriched in tumor‑associated processes, including 'Wnt signaling pathway', 'Notch signaling pathway', 'cell adhesion molecules' and 'extracellular matrix organization'. Chromatin immunoprecipitation sequencing revealed widespread ΔNp63α binding in promoter‑proximal and ‑distal regulatory regions, suggesting potential involvement in transcriptional regulation through both proximal and distal genomic elements. ΔNp63α upregulation was also associated with increased CCCTC‑binding factor (CTCF) occupancy near the promoters of tumor‑associated genes and these gained CTCF sites were enriched for p63 motifs. Collectively, the present findings identified ΔNp63α as an oncogenic regulator of HCC and suggest that it may regulate tumor‑associated gene programs through coordinated proximal and distal chromatin regulatory mechanisms.
SN - 1791-2997
SN - 1791-3004
ER -