Comparative Proteomic Analysis of Indioside D-Triggered Cell Death in HeLa Cells

2008 ◽  
Vol 7 (5) ◽  
pp. 2050-2058 ◽  
Author(s):  
Chi Chun Wong ◽  
Ying Wang ◽  
Ka-Wing Cheng ◽  
Jen-Fu Chiu ◽  
Qing-Yu He ◽  
...  
2021 ◽  
Vol 22 (12) ◽  
pp. 6323
Author(s):  
Alexander L. Rusanov ◽  
Peter M. Kozhin ◽  
Olga V. Tikhonova ◽  
Victor G. Zgoda ◽  
Dmitry S. Loginov ◽  
...  

In vitro models are often used for studying macrophage functions, including the process of phagocytosis. The application of primary macrophages has limitations associated with the individual characteristics of animals, which can lead to insufficient standardization and higher variability of the obtained results. Immortalized cell lines do not have these disadvantages, but their responses to various signals can differ from those of the living organism. In the present study, a comparative proteomic analysis of immortalized PMJ2-R cell line and primary peritoneal macrophages isolated from C57BL/6 mice was performed. A total of 4005 proteins were identified, of which 797 were quantified. Obtained results indicate significant differences in the abundances of many proteins, including essential proteins associated with the process of phagocytosis, such as Elmo1, Gsn, Hspa8, Itgb1, Ncf2, Rac2, Rack1, Sirpa, Sod1, C3, and Msr1. These findings indicate that outcomes of studies utilizing PMJ2-R cells as a model of peritoneal macrophages should be carefully validated. All MS data are deposited in ProteomeXchange with the identifier PXD022133.


Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 534
Author(s):  
Sucharat Tungsukruthai ◽  
Onrapak Reamtong ◽  
Sittiruk Roytrakul ◽  
Suchada Sukrong ◽  
Chanida Vinayanwattikun ◽  
...  

Autophagic cell death (ACD) is an alternative death mechanism in resistant malignant cancer cells. In this study, we demonstrated how polyphenol stilbene compound PE5 exhibits potent ACD-promoting activity in lung cancer cells that may offer an opportunity for novel cancer treatment. Cell death caused by PE5 was found to be concomitant with dramatic autophagy induction, as indicated by acidic vesicle staining, autophagosome, and the LC3 conversion. We further confirmed that the main death induction caused by PE5 was via ACD, since the co-treatment with an autophagy inhibitor could reverse PE5-mediated cell death. Furthermore, the defined mechanism of action and upstream regulatory signals were identified using proteomic analysis. Time-dependent proteomic analysis showed that PE5 affected 2142 and 1996 proteins after 12 and 24 h of treatment, respectively. The crosstalk network comprising 128 proteins that control apoptosis and 25 proteins involved in autophagy was identified. Protein–protein interaction analysis further indicated that the induction of ACD was via AKT/mTOR and Bcl-2 suppression. Western blot analysis confirmed that the active forms of AKT, mTOR, and Bcl-2 were decreased in PE5-treated cells. Taken together, we demonstrated the novel mechanism of PE5 in shifting autophagy toward cell death induction by targeting AKT/mTOR and Bcl-2 suppression.


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