ArticleHuman cell2021
STAT3 inhibitor BBI608 enhances the antitumor effect of gefitinib on EGFR-mutated non-small cell lung cancer cells.
Article in Human cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Downregulation of RORl via STAT3 and P300 Promotes P38 Pathway- Dependent Lens Epithelial Cells Apoptosis in Age-Related Cataract.Biochemical genetics · 2026Article
- Ascomycin enhances the antitumor activity of osimertinib in EGFR-TKI-resistant non-small cell lung cancer.Frontiers in oncology · 2026Article
- Article
- Tumor-associated macrophages mediate resistance of EGFR-TKIs in non-small cell lung cancer: mechanisms and prospects.Frontiers in immunology · 2023Review
- Nanoparticle-Mediated Delivery of STAT3 Inhibitors in the Treatment of Lung Cancer.Pharmaceutics · 2022Review
- The Ror-Family Receptors in Development, Tissue Regeneration and Age-Related Disease.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib is known as epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) while an increasing number of patients with non-small cell lung cancer (NSCLC) are becoming resistant to EGFR-TKI. Therefore, innovative methods are urgently needed to overcome primary and acquired resistance to EGFR-TKIs in NSCLC patients. The viability of HCC827 cells and HCC827 Ge-resistant (Ge-r) cells treated with gefitinib and/or STAT3 inhibitor and/or Overexpression (Oe)-ROR1 was detected by CCK-8 assay. The colony formation, invasion, migration and apoptosis of HCC827 Ge-r cells treated with gefitinib and/or STAT3 inhibitor and/or Oe-ROR1 transfection were, respectively, detected by clone formation assay, transwell assay, wound healing assay and flow cytometry analysis. The protein expressions of EGFR, STAT3, invasion and migration-related proteins, ROR1/ABCB1/P53 pathway and apoptosis-related proteins were analyzed by Western blot analysis. The transfection effect of Oe-ROR1 in HCC827 Ge-r cells was confirmed by qRT-PCR and Western blot analysis. In vivo animal experiment was used to confirm the role of STAT3 in improving the sensitivity of HCC827 Ge-r cells to gefitinib. As a result, after treatment of gefitinib, the viability of HCC827 cells was lower than that of HCC827 Ge-r cells and the expression of p/t-EGFR and p/t-STAT3 was decreased in HCC827 cells and HCC827 Ge-r cells after treatment of gefitinib. STAT3 inhibitor BBI608 enhanced the ability of gefitinib to inhibit viability, invasion and migration while promoting apoptosis of HCC827 Ge-r cells treated with gefitinib, which was partially reversed by ROR1 overexpression. STAT3 inhibitor further down-regulated the expression of MMP2, MMP9, ROR1, ABCB1 and BCl2, while up-regulated the expression of p53, bax and cleaved caspase3 in HCC827 Ge-r cells treated with gefitinib, which was partially reversed by ROR1 overexpression. In vivo experiment, STAT3 inhibitor further suppressed the size of NSCLC tissues, and further down-regulated the expression of ROR1 and ABCB1 while up-regulated the expression of p53 in NSCLC tissues. In conclusion, STAT3 inhibitor enhanced the antitumor effect of gefitinib on EGFR-mutated NSCLC cells through regulating ROR1/ABCB1/P53 pathway.
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