Bufalin induces apoptosis of HCT116 cells by activating endoplasmic reticulum stress pathway
10.19405/j.cnki.issn1000-1492.2023.02.018
- Author:
Jing Shang
1
,
2
,
3
;
Zongheng Li
1
,
2
,
3
;
Qi Xia
3
,
4
;
Donghao Tang
1
,
2
,
3
;
Jia Chen
3
,
4
;
Zeting Yuan
3
,
4
;
Peihao Yin
1
,
2
,
5
,
6
Author Information
1. Shanghai Putuo Central School of Clinical Medicine，Anhui Medical University，Shanghai 200062
2. The Fifth School of Clinical Medicine，Anhui Medical University，Hefei 230032
3. Interventional Cancer Institute of Chinese Integrative Medicine，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
4. Dept of General Surgery， Putuo Hospital，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
5. Dept of General Surgery， Putuo Hospital，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
6. Interventional Cancer Institute of Chinese Integrative Medicine，Shanghai University of Traditional Chinese Medicine，Shanghai 200062
- Publication Type:Journal Article
- Keywords:
bufalin;
endoplasmic reticulum stress;
cell apoptosis;
colorectal cancer
- From:
Acta Universitatis Medicinalis Anhui
2023;58(2):274-279
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To study the effect of bufalin on the proliferation and apoptosis of human colorectal cancer cell line HCT116，and to explore the role of endoplasmic reticulum stress ( ERS) in this process．
Methods :The effect of bufalin on the proliferation of HCT116 cells was determined by CCK-8 assay．After HCT116 cells were treated with different concentrations of bufalin for 48 hours，cell apoptosis was detected by Annexin V / PI assay， and the expression of apoptosis-related proteins Bax and Bcl-2 was detected by Western blot．At the same time，the expression of ERS-related proteins glucose regulated protein 78 ( GRP78) ，phosphorylated protein kinase R like endoplasmic reticulum kinase ( p-PERK) ，eukaryotic translation initiation factor 2 α ( eIF2 α) ，phosphorylated eukaryotic translation initiation factor 2 α (p-eIF2 α) and C / EBP homologous protein ( CHOP) was detected by Western blot．HCT116 cells were divided into control group，bufalin group and combination group (bufalin + 4-phenylbutyric acid) ，and the expression of apoptosis-related proteins Bax and Bcl-2 was observed by Western blot.
Results:CCK-8 assay showed that bufalin could inhibit the proliferation of HCT116 cells．Apoptosis assay showed that bufalin could induce apoptosis of HCT116 cells．The results of Western blot showed that bufalin could up-regulate the expression of pro-apoptotic protein Bax and down-regulate the expression of anti-apoptotic protein Bcl-2．It could also induce ERS and activate PERK / eIF2 α/ CHOP pathway．When bufalin combined with 4-phenylbutyric acid，the apoptosis-promoting effect of bufalin was inhibited．
Conclusion:Bufalin can effectively inhibit the prolif- erative activity and induce apoptosis of HCT116，which is achieved to some extent by activating ERS.
- Full text:2024071422161071770蟾毒灵通过激活内质网应激通路诱导HCT116细胞凋亡_尚靖.pdf
