ArticleInternational journal of biological sciences2026
HDAC1 Regulates Acquired Resistance to EGFR Inhibitors through the TFCP2-NDRG1 Signaling Axis in Pancreatic Cancer.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Epidermal growth factor receptor (EGFR) is a pivotal therapeutic target in pancreatic ductal adenocarcinoma (PDAC); however, the clinical efficacy of tyrosine kinase inhibitors (TKIs) such as erlotinib is frequently curtailed by acquired resistance. This study identifies histone deacetylase 1 (HDAC1) as a critical epigenetic driver of this resistance. HDAC1 is markedly upregulated in erlotinib-resistant PDAC cells, where it directly suppresses the transcriptional activity of TFCP2 through site-specific deacetylation at lysine 256 (K256). This modification attenuates TFCP2 function, leading to transcriptional repression of the metastasis suppressor NDRG1 and increased expression of EGFR, thereby activating EGFR-TKI resistance signaling pathways. Furthermore, EGFR-mediated tyrosine phosphorylation protects HDAC1 from ubiquitin-proteasome system (UPS)-dependent degradation, stabilizing HDAC1 and establishing a self-reinforcing feedback loop that sustains its elevated expression in the resistant state. To counter this mechanism, we designed a bioactive peptide derived from TFCP2 that competitively inhibits K256 deacetylation, thereby restoring TFCP2 transcriptional activity. In
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