scholarly journals Ellagic acid induces HeLa cell apoptosis via regulating signal transducer and activator of transcription 3 signaling

Author(s):  
Lian‑Wei Li ◽  
Chao Na ◽  
Song‑Yu Tian ◽  
Jie Chen ◽  
Rong Ma ◽  
...  
Metabolism ◽  
2010 ◽  
Vol 59 (3) ◽  
pp. 343-349 ◽  
Author(s):  
Phuong T. Hoang ◽  
Patricia Park ◽  
Laura J. Cobb ◽  
Valdislava Paharkova-Vatchkova ◽  
Michael Hakimi ◽  
...  

Author(s):  
Jinyu Xia ◽  
Chunyu Xue ◽  
Jie Yu

IntroductionEllagic acid (EA) is a kind of herb extract. However, the effects and mechanisms of EA in cervical cancer treatment are unclear.Material and methodsOur present work investigated the effects of EA on HeLa cervical cancer cell biological activities and relative mechanisms. Hela cells were divided into 5 groups as the NC group, Low group, Middle group, High group and 5-Fu group. MTT assay and cell apoptosis assay were performed to evaluate cell proliferation and apoptosis. Wound closure assay was used to assess the effect of EA on HeLa cell migration. We also assessed the anti-tumor effect of EA on a cervical tumor bearing BALB/c mouse model. Furthermore, western blotting and immunohistochemistry assay were performed to evaluate the effect of EA on the activation of AKT/mTOR/STAT3 in vitro and in vivo.ResultsThe cell experiments showed that EA had effects to inhibit Hela cell biological activities including cell apoptosis, migration and invasion dose-dependently and AKT, mTOR, and STAT3 phosphorylation expression levels were significantly depressed after EA supplementation in the in vitro study. In the in vivo study, EA significantly depressed tumor growth with cell apoptosis significantly increasing and the AKT/mTOR/STAT3 pathway was significantly down-regulated in tumor tissues.ConclusionsEA had anti-tumor effects on cervical cancer by depressing the AKT/mTOR/STAT3 pathway in in vitro and in vivo study.


2021 ◽  
Vol 19 (4) ◽  
pp. 458-463
Author(s):  
Jing Yue ◽  
Hong Zhou ◽  
Zhenzhen Jiang

Sepsis is a systemic response to infections that may culminate into a life-threatening syndrome, the most common cause of acute kidney injury. Despite increasing mortality associated with septic acute kidney injury, its pathogenesis is poorly understood resulting in limited treatment options. Amygdalin participates in the regulation of various signaling pathways including Janus kinase/signal transducer and activator of transcription 3 signaling pathway. This pathway is critical for initiating immune responses and controlling persistent inflammation in various conditions such as infection. Cecal ligation and puncture is a most frequently used method for modeling sepsis. In the rat cecal ligation and puncture model, the levels of serum creatinine and blood urea nitrogen, as well as the serum levels of proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, and interleukin-18) are significantly elevated. Furthermore, cecal ligation and puncture promotes cell apoptosis with increased BCL2-associated X protein and reduced B-cell lymphoma 2 protein expression. In this study, we have observed amygdalin to reduce serum cytokine secretion and prevent renal cell apoptosis in kidney injury, thus ameliorate kidney injury. The protective role of amygdalin in septic acute kidney injury was mediated through inhibition of Janus kinase/signal transducer and activator of the transcription 3 signaling pathway.


2017 ◽  
Author(s):  
I Silva ◽  
V Rausch ◽  
T Peccerella ◽  
G Millonig ◽  
HK Seitz ◽  
...  

2019 ◽  
Vol 19 (10) ◽  
pp. 817-827
Author(s):  
Jianbo Zhu ◽  
Lijuan Deng ◽  
Baozhen Chen ◽  
Wenqing Huang ◽  
Xiandong Lin ◽  
...  

Background:Recurrence is the leading cause of treatment failure and death in patients with gastric cancer (GC). However, the mechanism underlying GC recurrence remains unclear, and prognostic markers are still lacking.Methods:We analyzed DNA methylation profiles in gastric cancer cases with shorter survival (<1 year) or longer survival (> 3 years), and identified candidate genes associated with GC recurrence. Then, the biological effects of these genes on gastric cancer were studied.Results:A novel gene, magnesium-dependent phosphatase 1 (mdp1), was identified as a candidate gene whose DNA methylation was higher in GC samples from patients with shorter survival and lower in patients with longer survival. MDP1 protein was highly expressed in GC tissues with longer survival time, and also had a tendency to be expressed in highly differentiated GC samples. Forced expression of MDP1 in GC cell line BGC-823 inhibited cell proliferation, whereas the knockdown of MDP1 protein promoted cell growth. Overexpression of MDP1 in BGC-823 cells also enhanced cell senescence and apoptosis. Cytoplasmic kinase protein c-Jun N-terminal kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) were found to mediate the biological function of MDP1.Conclusion:These results suggest that MDP1 protein suppresses the survival of gastric cancer cells and loss of MDP expression may benefit the recurrence of gastric cancer.


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