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McClellanville Library
Closed for renovations
Phone: (843) 887-3699
Miss Jane's Building (Edisto Library Temporary Location)
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Phone: (843) 869-2355
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St. Paul's/Hollywood Library
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Sesamol regulates autophagy and apoptosis of esophageal squamous cell carcinoma Eca109 cells through AMPK/SIRT1/NF-kB signal pathway. (English)
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- Author(s): LIU Shan; WANG Huabing; LIU Chong; ZHANG Zhuo
- Source:
Chinese Journal of Cancer Biotherapy; 2023, Vol. 30 Issue 2, p123-128, 6p- Subject Terms:
- Source:
- Additional Information
- Abstract: Objective: To explore the effect of sesamol (SEM) on autophagy and apoptosis of esophageal squamous cell carcinoma (ESCC) Eca109 cells through adenylate activated protein kinase (AMPK)/silencing information regulator 1 (SIRT1)/nuclear factor kB (NF-kB) pathway. Methods: Eca109 cells of ESCC and HEEpiC of human esophageal epithelial cells were treated with different concentrations of SEM (0, 1.562 5, 3.125, 6.25, 12.5, 25, 50, 100, 200, and 400 μmol/L) for 48 hours. Cell viability was detected by CCK-8 method and appropriate SEM concentrations were screened for subsequent experiments. Eca109 cells were grouped into control group (CK group, 0 µmol/L), low-dose SEM group (SEM-L group, 25 µmol/L), medium-dose SEM group (SEM-M group, 50 µmol/L), high-dose SEM group (SEM-Mgroup, 50 µmol/L), high-dose SEM group (SEM-Hgroup, 100 µmol/L) and high-dose SEM+compound C (AMPK inhibitor) group (SEM-H+Compound C group, 100 µmol/L+10 µmol/L). All Eca109 cells were treated at the corresponding drug concentration for 48 hours. CCK-8 assay was applied to detect the proliferation of Eca109 cells; flow cytometry was applied to detect apoptosis; transmission electron microscopy was applied to observe autophagosomes in Eca109 cells and WB assay was applied to detect the protein expressions of microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I, Beclin-1, B-lymphoma-2 (Bcl2), Bcl2-associated X protein (BAX), p-AMPK, SIRT1, p-NF-kB p65 in Eca109 cells 2. Results: The SEM concentrations of 25, 50 and 100 μmol/L selected through pre-experiment are used for formal research. Under SEM processing, compared with the CK group, the proliferation levels (24, 48 h) of Eca109 cells, protein expressions of Bcl2 and p-NF-kB p65 in SEM-L group, SEM-M group and SEM-Hgroup decreased significantlywhile the apoptosis rate, the number of autophagosomes, the protein expressions of LC3II-/LC3-I, Beclin-1, BAX, p-AMPK and SIRT1 increased significantly, in a dose-dependent manner (all P<0.05); compared with the SEM-H group, the proliferation level (24, 48 h) of Eca109 cells, protein expressions of Bcl2 and p-NF-kB p65 in SEM-H+Compound C group increased significantly while the apoptosis rate, the number of autophagosomes, the protein expressions of LC3II-/LC3-I, Beclin-1, BAX, p-AMPK and SIRT1 decreased significantly(all P<0.05). Conclusion: SEM may promote autophagy and apoptosis of Eca109 cells by activating AMPK/SIRT1 signaling pathway and inhibiting NF-kB vitality. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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