Co-administration of apigenin with doxorubicin enhances anti-migration and antiproliferative effects via PI3K/PTEN/AKT pathway in prostate cancer cells

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dc.authorscopusid57225995507
dc.authorscopusid57226002747
dc.authorscopusid56888820000
dc.authorscopusid7004540505
dc.contributor.authorAyyildiz A.
dc.contributor.authorKoc H.
dc.contributor.authorTurkekul K.
dc.contributor.authorErdogan S.
dc.date.accessioned2024-06-12T10:25:58Z
dc.date.available2024-06-12T10:25:58Z
dc.date.issued2021
dc.description.abstractProstate cancer is one of the leading cancers in men, and new approaches are needed for its treatment. The aim of this study was to investigate the effect of co-administration of naturally occurring flavone apigenin and doxorubicin to androgen-insensitive prostate cancer cells. Methods: The effect of the treatment on survival and migration of human PC3 cells was evaluated by MTT and scratch assay, respectively. Apoptosis and cell cycle distribution were detected by image-based cytometry. mRNA and protein expression were determined by real-time quantitative polymerase chain reaction and Western blot, respectively. Results: Apigenin and doxorubicin dose-dependently inhibited cell survival, and co-administration of both agents significantly induced cell death via upregulating the mRNA expression of caspases, Bax and cytochrome c, and downregulating Bcl-XL. Combination therapy caused cell cycle arrest by upregulating the expression of p21 and p27. The treatment modality inhibited cell migration via downregulating Snail, Twist and MMPs in which doxorubicin was ineffective. Apigenin dephosphorylated Akt strongly, significantly suppressed ERK phosphorylation, and increased PTEN expression 4.5-fold. The combination of apigenin and doxorubicin inhibited PI3K and AKT phosphorylation more strongly than a single administration. Conclusions: Our data indicate that a combination of the natural flavone apigenin with doxorubicin might have a potential in treatment of castration-resistant prostate cancer. Copyright © Experimental Oncology, 2021en_US
dc.description.sponsorshipTrakya Üniversitesi: 2018 — 17en_US
dc.description.sponsorshipThis study was funded by the Trakya University Research Project Foundation (TUBAP: 2018 — 17).en_US
dc.identifier.doi10.32471/exp-oncology.2312-8852.vol-43-no-2.16096
dc.identifier.endpage134en_US
dc.identifier.issn1812-9269
dc.identifier.issue2en_US
dc.identifier.pmid34190523en_US
dc.identifier.scopus2-s2.0-85110067485en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage125en_US
dc.identifier.urihttps://doi.org/10.32471/exp-oncology.2312-8852.vol-43-no-2.16096
dc.identifier.urihttps://hdl.handle.net/20.500.14551/16600
dc.identifier.volume43en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherMorion LLCen_US
dc.relation.ispartofExperimental Oncologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectApigenin; Cell Migration; Doxorubicin; Pc3; Prostate Canceren_US
dc.subjectApigenin; Caspase; Cytochrome C; Doxorubicin; Matrix Metalloproteinase; Messenger Rna; Phosphatidylinositol 3 Kinase; Phosphatidylinositol 3,4,5 Trisphosphate 3 Phosphatase; Protein Bax; Protein Bcl Xl; Protein Kinase B; Protein P21; Protein P27; Transcription Factor Snail; Transcription Factor Twist; Antineoplastic Agent; Apigenin; Doxorubicin; Phosphatidylinositol 3 Kinase; Phosphatidylinositol 3,4,5 Trisphosphate 3 Phosphatase; Protein Kinase B; Pten Protein, Human; Antiproliferative Activity; Apoptosis; Article; Cancer Cell; Cell Cycle Arrest; Cell Death; Cell Migration; Cell Survival; Controlled Study; Cytometry; Dose Response; Down Regulation; Drug Effect; Gene Expression; Human; Human Cell; Mtt Assay; Pc-3 [Human Prostate Carcinoma] Cell Line; Prostate Cancer; Protein Dephosphorylation; Protein Expression; Protein Phosphorylation; Real Time Polymerase Chain Reaction; Signal Transduction; Upregulation; Western Blotting; Wound Healing Assay; Castration Resistant Prostate Cancer; Cell Motion; Cell Proliferation; Drug Effect; Male; Pathology; Signal Transduction; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apigenin; Cell Movement; Cell Proliferation; Doxorubicin; Humans; Male; Pc-3 Cells; Phosphatidylinositol 3-Kinases; Prostatic Neoplasms, Castration-Resistant; Proto-Oncogene Proteins C-Akt; Pten Phosphohydrolase; Signal Transductionen_US
dc.titleCo-administration of apigenin with doxorubicin enhances anti-migration and antiproliferative effects via PI3K/PTEN/AKT pathway in prostate cancer cellsen_US
dc.title.alternative??????? ???????? ????????? ? ?????????????? ???????? ??????????????? ?? ??????????????????? ?????? ????? PI3K/PTEN/AKT ????? ? ???????? ???? ?????????????? ??????en_US
dc.typeArticleen_US

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