ArticleBBA advances2026
CEMIP promotes gefitinib resistance in lung cancer with EGFR-mutation possibly through forming a stable complex CEMIP/c-MYC.
Article in BBA advances, 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
While gefitinib greatly improves the prognosis of lung cancer patients with epidermal growth factor receptor (EGFR) mutation, its inevitable resistance severely diminishes therapeutic efficacy. Cell migration-inducing protein (CEMIP) might interact with cellular MYC proto-oncogene (c-MYC) to synergistically drive gefitinib resistance. However, the mechanism by which CEMIP/c-MYC regulates gefitinib resistance in LUAD remains unknown. The gefitinib-acquired resistance (AR) cell line PC9GR was established by gradual dose-escalation induction. CEMIP expression was up-regulated in PC9GR cells, suggesting the positive corelationship might exsit between CEMIP expression and gefitinib resistance. Similarly, overexpressing CEMIP in PC9 cells not only increased IC
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