The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells

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dc.contributor.authorÇetintaş, Vildan Bozok
dc.contributor.authorDüzgün, Zekeriya
dc.contributor.authorDoğan, Eda
dc.contributor.authorYıldırım, Zafer
dc.contributor.authorÖzdil, Berrin
dc.contributor.authorAktuğ, Hüseyin
dc.date.accessioned2023-01-12T20:37:34Z
dc.date.available2023-01-12T20:37:34Z
dc.date.issued2021
dc.departmentN/A/Departmenten_US
dc.description.abstractPIKfyve is an evolutionarily conserved lipid and protein kinase enzyme that has pleiotropic cellular functions. The aim of the present study was to investigate the effects of phosphatidylinositol-3-phosphate 5-kinase (PIKfyve) inhibitor, YM201636, on nonsmall cell lung cancer (NSCLC) cells growth, tumorigenicity, and claudin (CLDN) expressions. Three NSCLC cell lines (Calu-1, H1299 and HCC827) were used to compare the effects of YM201636. Cytotoxic effects of YM201636 were analysed using XTT assay. Malignancy potential of cells assesses with wound healing and soft agar colony-forming assays. mRNA and protein expressions of claudins were analysed by qRT-PCR and immunofluorescence staining. Our results revealed that YM201636 inhibited the proliferation and malignancy potential of Calu-1, H1299, and HCC827 cells in a dose-dependent manner. After YM201636 treatment CLDN1, -3 and -5 expressions increased significantly in HCC827 cells. CLDN3 and -5 expressions also significantly increased in Calu-1 cell line. YM201636 treatment significantly reduced the CLDN1 and increased the CLDN5 expression in H1299 cells. Immunofluorescence staining of CLDN1, -3 and -5 proteins showed a significant increase after YM201636 treatment. Besides, YM201636 induced EGFR mRNA expression in all NSCLC cell lines. Our results have shown that YM201636 inhibits tumorigenicity of NSCLC cells. Furthermore, estimated glomerular filtration rate (EGFR) pathway is important signalling involved in the regulation of claudins. Understanding the mechanisms of PIKfyve inhibitors may improve cancer treatment particularly for EGFR overactivated NSCLC.en_US
dc.identifier.endpage34en_US
dc.identifier.issn1300-0152
dc.identifier.issn1303-6092
dc.identifier.issue1en_US
dc.identifier.startpage26en_US
dc.identifier.trdizinid433696en_US
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/433696
dc.identifier.urihttps://hdl.handle.net/11454/81709
dc.identifier.volume45en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofTurkish Journal of Biologyen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectnonsmall cell lung canceren_US
dc.subjectClaudinen_US
dc.subjectepidermal growth factor receptoren_US
dc.subjectYM201636en_US
dc.subjectPIKfyveen_US
dc.titleThe effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cellsen_US
dc.typeArticleen_US

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