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Chloroquine inhibits viability of renal carcinoma cells and enhances sunitinib-induced caspase-dependent apoptosis
Ist Teil von
Beijing da xue xue bao. Journal of Peking University. Yi xue ban, 2018-10, Vol.50 (5), p.778
Ort / Verlag
China
Erscheinungsjahr
2018
Quelle
MEDLINE
Beschreibungen/Notizen
To determine whether chloroquine (CQ), an often used inhibitor of late autophagy and autophagosome/lyosome fusion, can inhibit proliferation of renal carcinoma cells and investigate its effect on sunitinib (ST)-induced apoptosis.
Renal carcinoma cell line 786 O and ACHN had been used as cellular model and 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS) assay was carried out to detect the cell viability in response to CQ or ST treatment. Both transmission electron microscope and immunoblotting had been employed to observe apoptotic and autophagic process. To examine the involvement of autophagy in ST-dependent apoptosis, autophagy had been inhibited either chemically or genetically via utilizing autophagy inhibitor or specific small interference RNA (siRNA) targeted to either Ulk1 (unc-51-like kinase 1) or LC3 (microtubule associated protein 1 light chain 3 fusion protein), two essential autophagic proteins.
Both ST and CQ induced cell viability loss,