ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2025
PSIP1 promotes gefitinib resistance in lung adenocarcinoma by inducing the expression of WASF3 and its downstream ITGB3/AKT signaling.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- The Acidic Exosomal miR-1246/WASF3 Axis Regulates Hepatic Stellate Cell Activation and Stiff ECM Remodeling to Promote Pancreatic Ductal Adenocarcinoma Liver Metastasis.International journal of biological sciences · 2026Article
- Chromatin-focused genetic and chemical screens identify BRPF1 as a targetable vulnerability in Taxol-resistant triple-negative breast cancer.Experimental & molecular medicine · 2025Article
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Abstract
backgroundGefitinib (GR), a representative drug of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is a key pillar in the treatment of lung adenocarcinoma (LUAD), but drug resistance is universal. Identifying the potential factors of drug resistance to GR is essential to treat patients with EGFR mutant LUAD.
methodsThe GR-resistant LUAD cells were established and confirmed by MTT assay. The effects of PC4 and SRSF1 interacting protein 1 (PSIP1) on GR-resistant cell proliferation and apoptosis in vitro and in vivo were detected by colony formation, flow cytometry, tumor-bearing animal model, immunohistochemistry, and TUNEL staining. Western blotting and qPCR were used to determine the expression of relevant markers. The effect of PSIP1 on the promoter region of Wiskott-Aldrich syndrome protein family member 3 (WASF3) was detected by the dual-luciferase assay. The interaction between PSIP1 and RNA polymerase II was evaluated using ChIP-qPCR and Co-IP assays.
resultsPSIP1 was highly enriched in GR-resistant LUAD cells. Downregulation of PSIP1 expression significantly inhibited the proliferation of LUAD-resistant cells and promoted apoptosis. WASF3 was shown to have similar effects as PSIP1 in promoting drug resistance in LUAD cells. PSIP1 promoted the transcriptional activity of WASF3, which was achieved by increasing RNA polymerase II recruitment on the WASF3 promoter. Furthermore, PSIP1 positively regulated the expression of the pro-EGFR-TKI resistance factor integrin subunit beta 3 (ITGB3).
conclusionOur work suggests that PSIP1 promotes resistance to GR in LUAD cells by inducing the expression of WASF3 and its downstream regulator ITGB3.
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