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Erdafitinib exerts the anticancer effect on urothelial carcinoma via induction of authophagy
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Erdafitinib has recently been approved for the treatment of adult patients with locally advanced or metastatic urothelial carcinoma (UC). The current study aimed to evaluate whether erdafitinib inhibits the proliferation in UC via inducing authophagy. Our data showed that erdafitinib demonstrated strong toxicity for the T24 and UMUC6 cell lines. Flow cytometry analysis showed that erdafitinib increased the proportion of G0/G1 phase in both T24 and UMUC6 cells. Additionally, Annexin V staining indicated that erdafitinib enhanced the apoptosis of UC cells. Meanwhile, the expression of apoptosis-related proteins was significantly elevated after treatment with erdafitinib. Transwell assay showed that erdafitinib significantly reduced T24 and UMUC6 cell migration and invasion. More importantly, western blot assay showed that erdafitinib induced the expression of autophagy-related proteins. Besides, GFP-LC3 transfection assay and electron microscopy examination showed that erdafitinib could partially diminish 3-methyladenine (3-MA) induced impairment of autophagy in UC cells. In summary, for the first time we showed novel data that erdafitinib inhibited UC cell malignant proliferation via inducing cell autophagy.
Title: Erdafitinib exerts the anticancer effect on urothelial carcinoma via induction of authophagy
Description:
Erdafitinib has recently been approved for the treatment of adult patients with locally advanced or metastatic urothelial carcinoma (UC).
The current study aimed to evaluate whether erdafitinib inhibits the proliferation in UC via inducing authophagy.
Our data showed that erdafitinib demonstrated strong toxicity for the T24 and UMUC6 cell lines.
Flow cytometry analysis showed that erdafitinib increased the proportion of G0/G1 phase in both T24 and UMUC6 cells.
Additionally, Annexin V staining indicated that erdafitinib enhanced the apoptosis of UC cells.
Meanwhile, the expression of apoptosis-related proteins was significantly elevated after treatment with erdafitinib.
Transwell assay showed that erdafitinib significantly reduced T24 and UMUC6 cell migration and invasion.
More importantly, western blot assay showed that erdafitinib induced the expression of autophagy-related proteins.
Besides, GFP-LC3 transfection assay and electron microscopy examination showed that erdafitinib could partially diminish 3-methyladenine (3-MA) induced impairment of autophagy in UC cells.
In summary, for the first time we showed novel data that erdafitinib inhibited UC cell malignant proliferation via inducing cell autophagy.
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