ArticleFrontiers in oncology2025
Targeting endoplasmic reticulum stress-induced CLGN resensitizes hepatocellular carcinoma to apoptosis: paeonol synergistically enhances efficacy by dual inhibition of CLGN and NF-κB.
Article in Frontiers in oncology, 2025. 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
Purpose: Endoplasmic reticulum stress (ERS) drives hepatocellular carcinoma (HCC) progression and therapy resistance. This study identifies Calmegin (CLGN) as a novel ERS-induced pro-survival factor and explores shCLGN combined with Paeonol (Pae) to overcome apoptosis resistance via NF-κB suppression. Materials and methods: CLGN was discovered by transcriptome sequencing of tunicamycin (TM)-induced ERS in HepG2 cells and validated via Western blot. Clinical significance was assessed using 93 paired HCC/adjacent tissues (IHC/WB) and TCGA data. Functional roles of CLGN (proliferation: CCK-8/EdU; migration/invasion: Transwell; apoptosis: flow cytometry). shCLGN efficacy alone or with Pae was tested Results: ERS significantly upregulated CLGN in HCC, correlating with advanced tumor stage and poor prognosis. CLGN promoted proliferation/migration and suppressed apoptosis. Crucially, sh-CLGN sensitized HCC cells to Pae, synergistically enhancing apoptosis and tumor suppression. Mechanistically, CLGN sustained survival via NF-κB activation; the combination (sh-CLGN + Pae) dual-blocked CLGN/NF-κB, reversing pro-survival signaling Conclusion: CLGN is a pivotal ERS effector mediating HCC apoptosis resistance through NF-κB. Sh-CLGN combined with Pae restores apoptotic sensitivity via dual CLGN/NF-κB inhibition, providing a potent strategy against ERS-adapted HCC.
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