ArticleHepatology (Baltimore, Md.)2026
NEK7-induced phosphorylation of EGFR on serine 1070 drives the acquired lenvatinib resistance in hepatocellular carcinoma.
Article in Hepatology (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- DIXDC1 Promotes Lymphatic Metastasis and Resistance to Cuproptosis in Bladder Cancer Through Mediating DLAT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- CRISPR Screening in Hepatocellular Carcinoma: From Tumor Progression to Immune Evasion and Therapeutic Resistance.International journal of molecular sciences · 2026Review
- COLEC12high tumor-associated macrophages orchestrate lenvatinib resistance and cancer stemness in hepatocellular carcinoma via paracrine NRG1-HER2/HER3 signaling.Clinical and molecular hepatology · 2026Article
- Quercetin suppresses the progression of HBV-associated hepatocellular carcinoma by modulating the EGFR signaling pathway.PloS one · 2026Article
- Local therapy overcomes primary resistance to target-immunotherapy combination in unresectable hepatocellular carcinoma.Cancer immunology, immunotherapy : CII · 2025Article
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Authors and funding
18 authors.
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Abstract
BACKGROUND AND
aimsLenvatinib is recognized as a first-line therapy for inoperable hepatocellular carcinoma (HCC) patients. Growing evidence indicates that lenvatinib resistance can be acquired in HCC cells via kinase rewiring. APPROACH AND
resultsWe established acquired lenvatinib-resistant organoids and HCC cell lines. NIMA-related coiled-coil kinase 7 (NEK7) was identified as an HCC lenvatinib acquired resistance gene by kinase CRISPR-Cas9 genetic screen. Functional analyses demonstrate that NEK7 enhanced lenvatinib resistance in HCC, and NEK7 knockdown or knockout displays the antitumor effects in acquired lenvatinib HCC cells and organoids. Mechanistically, NEK7 binds to the endothelial growth factor receptor (EGFR), leading to the phosphorylation of EGFR specifically at the serine 1070 residue, which contributes to the activation of MAPK (mitogen-activated protein kinase) and PI3K/AKT (phosphoinositide 3-kinase/Akt) signaling pathways. Consistently, designed inhibitory peptides targeting the domain from amino acids 979 to 1099 were proven to inhibit phosphorylation of EGFR S1070 site and therapeutically inhibit antitumor activity of acquired lenvatinib resistance HCC.
conclusionsOur results unveil insights into the acquired lenvatinib resistance mechanism that NEK7 phosphorylates EGFR at S1070 to promote acquired lenvatinib resistance in HCC.
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