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- W2568510040 abstract "Epidermal growth factor receptor (EGFR)-driven lung cancers are among the most threatening malignancies with extremely high mortality. Despite the successful application of tyrosine kinase inhibitors (TKIs) in treating these carcinomas, the therapeutic efficacy of EGFR-TKIs has been compromised by frequently occurring drug resistance.The mechanisms that maintain cell survival and cause sustained proliferation upon TKI treatment remain to be fully understood. Cell culture, western blot, bioinformatic study, luciferase reporter assay and xenograft model study were employed in this study. In this study, we found that miR-26a was upregulated in some TKI-refractory NSCLC cells; miR-26a directly targets and silences protein tyrosine phosphatase non-receptor type 13 (PTPN13) to maintain the activation of Src, a dephosphorylation substrate of PTPN13. Whereas miR-26a is upregulated by EGFR signaling, EGFR/miR-26a/PTPN13/Src forms a feedforward circuit to reinforce EGFR pathway, which circumvents the complete suppression of EGFR signaling and cell proliferation by TKIs.View Large Image Figure ViewerDownload Hi-res image Download (PPT) In conclusion, our findings unraveled a novel mechanism underlying the resistance of lung cancers to TKIs, and thus have implications for miR-26a as a predictive biomarker and a synergistic target for EGFR-inhibiting therapy of lung cancers." @default.
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- W2568510040 date "2017-01-01" @default.
- W2568510040 modified "2023-09-29" @default.
- W2568510040 title "PUB065 miR-26a Desensitizes Non-Small Cell Lung Cancer Cells to Tyrosine Kinase Inhibitors by Targeting PTPN13" @default.
- W2568510040 doi "https://doi.org/10.1016/j.jtho.2016.11.2035" @default.
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