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Titanium-nanostructured and PEGylated Doxorubicin Diminish Chemotherapeutic Resistance in 3-Methylcholanthrene Renal Epithelial Cell Carcinoma via KRAS/FKBP5/P53/JAK2 Signaling
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Titanium-nanostructured and PEGylated Doxorubicin Diminish Chemotherapeutic Resistance in 3-Methylcholanthrene Renal Epithelial Cell Carcinoma via KRAS/FKBP5/P53/JAK2 Signaling
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Titanium-nanostructured and PEGylated Doxorubicin Diminish Chemotherapeutic Resistance in 3-Methylcholanthrene Renal Epithelial Cell Carcinoma via KRAS/FKBP5/P53/JAK2 Signaling
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Journal Article
Titanium-nanostructured and PEGylated Doxorubicin Diminish Chemotherapeutic Resistance in 3-Methylcholanthrene Renal Epithelial Cell Carcinoma via KRAS/FKBP5/P53/JAK2 Signaling
2023
Overview
Background and ObjectivesNanoparticle (NP) drug delivery systems have been developed recently to resolve the obstacle of drug resistance, contributing to the effective drug delivery to the target organ. A comparative study was carried out herein between doxorubicin (DOX), doxorubicin-loaded titanium NPs, DOX-loaded lactoferrin NPs, DOX-NPs, and PEGylated-doxorubicin (PEG-DOX) on the reno-carcinogenic impact of 3-methylcholanthrene (CA).MethodsIn-vivo models were exposed to CA at a dose of 50 mg/kg body weight and left for 3 months till the incidence of chronic kidney disease, followed by one month of treatment with the aforementioned nanomedicines.ResultsCA downregulated DOX resistance biomarkers, including the gene expression of KRAS, FKBP5, P53, and JAK2, and the kidney tumor marker arginase II. In addition, CA increased the levels of the kidney biomarkers creatinine and urea as well as the minerals chloride and magnesium. Decreased gene expression of FKBP5, KRAS, P53, and JAK2 was reversed after the treatment with DOX-loaded titanium NPs, DOX-NPs, DOX-loaded lactoferrin NPs, and PEG-DOX. PEG-DOX abolished the detrimental effects of CA via upregulating the gene expression of the immunophilin protein (FKBP5), the oncogene (KRAS), the tumor suppressor gene (P53), and JAK2, which indicate DOX drug resistance via regulating cell differentiation, division and apoptosis.ConclusionPEG-DOX restored renal function and resolved DOX resistance via KRAS, FKBP5, P53, and JAK2 signaling pathways manipulation; consequently, PEG-DOX may provide a useful adjunct treatment for chronic kidney disease.
