Allyl-isatin suppresses cell viability, induces cell cycle arrest, and promotes cell apoptosis in hepatocellular carcinoma HepG2 cells.
作者： Weihua Bian , Yukuan An , Huiqing Qu , Yue Yang , Junhou Yang
DOI: 10.1111/FCP.12193
关键词: Cell cycle 、 Viability assay 、 Acridine orange 、 Propidium iodide 、 Apoptosis 、 Biology 、 Cell biology 、 Molecular biology 、 Cell cycle checkpoint 、 Cell morphology 、 Annexin
摘要: Abstract The anticancer effect of the newly synthesized isatin derivative, N-allyl-isatin (Allyl-I), was evaluated in vitro with human hepatocellular carcinoma HepG2 cells. Cell viability detected by cell counting kit-8 (CCK8) assay. Acridine orange (AO)/ethidium bromide (EB) double staining used to observe morphology. Flow cytometry assess effects Allyl-I on cycle, apoptosis rate, and mitochondrial membrane potential (MMP). Western blot analysis performed detect influence Ally1-I expression cytochrome c (cyt c), Bax, Bcl-2, cleaved caspase-3. significantly inhibited a time- dose-dependent manner. can induce cycle arrest cells at G2/M phase. Apoptotic nuclear morphological changes were observed after AO/EB staining. Fluorescein isothiocyanate-conjugated Annexin V (Annexin V-FITC) propidium iodide (PI) showed that apoptotic rates increased presence Allyl-I. Rhodamine 123 indicated decrease MMP. also altered apoptosis-related proteins. Protein levels cyt caspase-3 upregulated following treatment. By contrast, Bcl-2/Bax ratio decreased. Results suggest suppresses viability, induces arrest, promotes Furthermore, induction might be correlated pathway.
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