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dc.contributor.authorKavakcioglu Yardimci, Berna
dc.contributor.authorOzgun Acar, Ozden
dc.contributor.authorSemiz, Asli
dc.contributor.authorSen, Alaattin
dc.date.accessioned2022-02-16T12:39:41Z
dc.date.available2022-02-16T12:39:41Z
dc.date.issued2021en_US
dc.identifier.issn1300-7467
dc.identifier.urihttps //doi.org/10.5505/tjo.2020.2380
dc.identifier.urihttps://hdl.handle.net/20.500.12573/1153
dc.descriptionThis study was supported by Scientific Research Projects Unit of Pamukkale University (PAU-BAP2019BSP008).en_US
dc.description.abstractOBJECTIVE Defects in apoptotic cell death which restrict the success of conventional cytotoxic therapies have pivotal roles in a number of pathological conditions including cancer. However, a novel drug class targeting pro-survival Bcl-2 protein family members has been developed with the understanding of the structures and interactions of Bcl-2 proteins. Within this new class, Bcl-2/Bcl-xL inhibitor Navitoclax and Bcl-2 specific inhibitor Venetoclax have been shown to demonstrate strong anticancer activities on several types of cancers. But their low affinity to other anti-apoptotic proteins limits their clinical usage. Here, we investigated the cytotoxic and apoptotic effects of Navitoclax/Venetoclax and their combinations with specific tyrosine kinase inhibitor Apatinib on estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 breast cancer cell lines. METHODS MTT assay was used for the evaluation of the inhibition of cancer cell proliferation. ELISA test and Quantitative real-time PCR assay was performed to determine the role of caspase-3, Bak, Bax, Bcl-2, Bcl-xL and Mcl-1 proteins in the inhibition of cell proliferation triggered by the tested agents. RESULTS We found that aggressive MDA-MB-231 cell line was more sensitive to all tested agents. Apatinib significantly enhanced Navitoclax/Venetoclax mediated inhibition of cell viability in both cancer cell lines despite up-regulation in the expression levels of Bcl-2 and Mcl-1 genes. We further demonstrated significant Bak/Bax and caspase-3 expression in less aggressive MCF-7 cells. CONCLUSION Our findings have impacts on Navitoclax/Venetoclax plus Apatinib based therapy for breast adenocarcinoma. On the other hand, further studies should be conducted to elucidate the mechanisms underlying synergistic effects of Navitoclax/Venetoclax plus Apatinib combinations.en_US
dc.description.sponsorshipPamukkale University PAU-BAP2019BSP008en_US
dc.language.isoengen_US
dc.publisherKARE PUBLCONCORD ISTANBUL, DUMLUPINAR MAH, CIHAN SK NO 15, B BLOK 162 KADIKOY, ISTANBUL, TURKEYen_US
dc.relation.isversionof10.5505/tjo.2020.2380en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectApatiniben_US
dc.subjectCytotoxicityen_US
dc.subjectVenetoclaxen_US
dc.subjectNavitoclaxen_US
dc.subjectApoptosis, Breast adenocarcinomaen_US
dc.titleApatinib Sensitizes Human Breast Cancer Cells against Navitoclax and Venetoclax Despite Up-regulated Bcl-2 and Mcl-1 Gene Expressionsen_US
dc.typearticleen_US
dc.contributor.departmentAGÜ, Yaşam ve Doğa Bilimleri Fakültesi, Moleküler Biyoloji ve Genetik Bölümüen_US
dc.contributor.institutionauthorSen, Alaattin
dc.identifier.volumeVolume 36 Issue 1 Page 8-16en_US
dc.relation.journalTURK ONKOLOJI DERGISI-TURKISH JOURNAL OF ONCOLOGYen_US
dc.relation.publicationcategoryMakale - Uluslararası - Editör Denetimli Dergien_US


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