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PLGA-Quercetin Nano-Formulation Inhibits Cancer Progression via Mitochondrial Dependent Caspase-3,7 and Independent FoxO1 Activation with Concomitant PI3K/AKT Suppression

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dc.contributor.authorYadav, Neera-
dc.contributor.authorTripathi, Amit Kumar-
dc.contributor.authorParveen, Amna-
dc.date.accessioned2022-08-07T02:40:08Z-
dc.date.available2022-08-07T02:40:08Z-
dc.date.created2022-07-27-
dc.date.issued2022-07-
dc.identifier.issn1999-4923-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85194-
dc.description.abstractQuercetin is one of the most important plant flavanols, having several pharmacological and biological uses. Quercetin (Q) is an extremely hydrophobic phytochemical and has poor intracellular absorption, which makes its use limited. Present research demonstrates that quercetin-loaded PLGA nanoparticles (PLGA-QNPs) could overcome its low hydrophilicity and improve its anti-cancer potential. PLGA nanoparticles loaded with Q were prepared by the solvent evaporation technique and its anticancer activity was examined in vitro as well as in vivo. The cell viability was assessed through MTT assay and apoptosis was assayed through Hoechst-PI and EB/AO double staining followed by mitochondrial damage through Mito-tracker RMX-Ros. Gene expression was examined through RT-PCR. Cell cycle arrest in G2/M phase was analyzed through FACS. The results obtained revealed that PLGA-QNPs significantly reduced the viability of human cervical and breast cancer cell lines. PLGA-QNPs induced apoptosis in human cervical cancer cells in a dose dependent manner. The gene expression of PI3K/AKT was down-regulated and FoxO1 was upregulated in PLGA-QNP-treated cells, which showed a high expression level of active Caspase-3 and 7, which are responsible for apoptosis. In addition, PLGA-QNPs reduced the average number of tumors and prolonged the tumor latency period in DMBA-induced mammary adenocarcinoma SD rats. These findings suggest that PLGA-QNPs inhibit cervical and breast cancer progression via mitochondrial dependent Caspase-3 and 7 and mitochondrial independent FoxO1 activation with concomitant suppression of the PI3K/AKT pathway. For future studies, we suggest that potential druggability efficacy and clinical development of anticancer PLGA-QNPs need to be evaluated intensely for successful anticancer drug development. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.-
dc.language영어-
dc.language.isoen-
dc.publisherMDPI-
dc.relation.isPartOfPharmaceutics-
dc.titlePLGA-Quercetin Nano-Formulation Inhibits Cancer Progression via Mitochondrial Dependent Caspase-3,7 and Independent FoxO1 Activation with Concomitant PI3K/AKT Suppression-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000833331400001-
dc.identifier.doi10.3390/pharmaceutics14071326-
dc.identifier.bibliographicCitationPharmaceutics, v.14, no.7-
dc.description.isOpenAccessY-
dc.identifier.scopusid2-s2.0-85132986990-
dc.citation.titlePharmaceutics-
dc.citation.volume14-
dc.citation.number7-
dc.contributor.affiliatedAuthorYadav, Neera-
dc.contributor.affiliatedAuthorParveen, Amna-
dc.type.docTypeArticle-
dc.subject.keywordAuthoranti-cancer-
dc.subject.keywordAuthordrug delivery-
dc.subject.keywordAuthorFoxO1-
dc.subject.keywordAuthorphytochemical-
dc.subject.keywordAuthorquercetin-
dc.subject.keywordPlusCELL-CYCLE ARREST-
dc.subject.keywordPlusDNA-DAMAGE-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusNANOPARTICLE-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordPlusP53-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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