Role of IL‐6‐mediated expression of NS5ATP9 in autophagy of liver cancer cells

2018 ◽  
Vol 233 (12) ◽  
pp. 9312-9319 ◽  
Author(s):  
Hongping Lu ◽  
Ming Han ◽  
Xiaoxue Yuan ◽  
Kelbinur Tursun ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Liver Cancer Cells

Relevance of mitochondrial dysfunction during Sorafenib-induced cell death in liver cancer cells. Role of oxidative and nitrogen reactive species

2021 ◽  
Vol 165 ◽  
pp. 54
Author(s):  
Patricia de la Cruz-Ojeda ◽  
M. Ángeles Rodríguez-Hernández ◽  
Elena Navarro-Villarán ◽  
Paloma Gallego ◽  
Pavla Staňková ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Reactive Species ◽  
Liver Cancer Cells ◽  
Nitrogen Reactive Species

scholarly journals A critical role of AMPK, and Akt, mTOR and Wnt survival signals for the growth control of colon and liver cancer cells with selenium

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Lee Yun‐Kyoung ◽  
Song Yi Park ◽  
Won Sup Lee ◽  
Young‐Joon Surh ◽  
Young‐Min Kim ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Critical Role ◽  
Growth Control ◽  
Liver Cancer Cells ◽  
Survival Signals

scholarly journals The Role of Exosomes in the Crosstalk between Adipocytes and Liver Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1988
Author(s):  
Leslimar Rios-Colon ◽  
Elena Arthur ◽  
Suryakant Niture ◽  
Qi Qi ◽  
John T. Moore ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Bioactive Materials ◽  
Liver Cancer Cells ◽  
Secreted Factors ◽  
Wide Range ◽  
Pathophysiological Role ◽  
Inflammatory State ◽  
Membrane Bound

Exosomes are membrane-bound extracellular vesicles (EVs) that transport bioactive materials between cells and organs. The cargo delivered by exosomes can alter a wide range of cellular responses in recipient cells and play an important pathophysiological role in human cancers. In hepatocellular carcinoma (HCC), for example, adipocyte- and tumor-secreted factors contained in exosomes contribute to the creation of a chronic inflammatory state, which contributes to disease progression. The exosome-mediated crosstalk between adipocytes and liver cancer cells is a key aspect of a dynamic tumor microenvironment. In this review, we summarize the role of increased adiposity and the role of adipocyte-derived exosomes (AdExos) and HCC-derived exosomes (HCCExos) in the modulation of HCC progression. We also discuss recent advances regarding how malignant cells interact with the surrounding adipose tissue and employ exosomes to promote a more aggressive phenotype.

Antiproliferative Effects of Thymoquinone in MCF-7 Breast and HepG2 Liver Cancer Cells: Possible Role of Ceramide and ER Stress

2020 ◽  
pp. 1-13
Author(s):  
Mutay Aslan ◽  
Ebru Afşar ◽  
Esma Kırımlıoglu ◽  
Tuğçe Çeker ◽  
Çağatay Yılmaz
Keyword(s):  
Liver Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Antiproliferative Effects ◽  
Liver Cancer Cells ◽  
Mcf 7

scholarly journals Role of the cystathionine β-synthase/H2S system in liver cancer cells and the inhibitory effect of quinolone-indolone conjugate QIC2 on the system

2017 ◽  
Vol 37 (5) ◽  
pp. 3001-3009 ◽  
Author(s):  
Huina Jia ◽  
Juan Ye ◽  
Jing You ◽  
Xiaoyan Shi ◽  
Wenyi Kang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Liver Cancer Cells

scholarly journals TRIB2 desensitizes ferroptosis via βTrCP-mediated TFRC ubiquitiantion in liver cancer cells

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Susu Guo ◽  
Yuxin Chen ◽  
Xiangfei Xue ◽  
Yueyue Yang ◽  
Yikun Wang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Adaptor Protein ◽  
Ros Generation ◽  
Iron Level ◽  
E3 Ligases ◽  
Labile Iron Pool ◽  
Liver Cancer Cells ◽  
Labile Iron

AbstractTribbles homolog 2 (TRIB2) is known to boost liver tumorigenesis via regulating Ubiquitin (Ub) proteasome system (UPS). At least two ways are involved, i.e., acts as an adaptor protein to modulate ubiquitination functions of certain ubiquitin E3 ligases (E3s) and reduces global Ub levels via increasing the proteolysis activity of proteasome. Recently, we have identified the role of TRIB2 to relieve oxidative damage via reducing the availability of Ub that is essential for the ubiquitination and subsequent degradation of Glutathione peroxidase 4 (GPX4). Although GPX4 is a critical antioxidant factor to protect against ferroptosis, the exact evidence showing that TRIB2 desensitizes ferroptosis is lacking. Also, whether such function is via E3 remains unclear. Here, we demonstrated that deletion of TRIB2 sensitized ferroptosis via lifting labile iron in liver cancer cells. By contrast, overexpression of TRIB2 led to the opposite outcome. We further demonstrated that transferrin receptor (TFRC) was required for TRIB2 to desensitize the cells to ferroptosis. Without TFRC, the labile iron pool could not be reduced by overexpressing TRIB2. We also found that beta-transducin repeat containing E3 ubiqutin protein ligase (βTrCP) was a genuine E3 for the ubiquitination of TFRC, and TRIB2 was unable to decline labile iron level once upon βTrCP was knocked out. In addition, we confirmed that the opposite effects on ferroptosis and ferroptosis-associated lipid reactive oxygen species (ROS) generation resulted from knockout and overexpression of TRIB2 were all indispensible of TFRC and βTrCP. Finally, we demonstrated that TRIB2 exclusively manipulated RSL3- and erastin-induced-ferroptosis independent of GPX4 and glutathione (GSH). In conclusion, we elucidated a novel role of TRIB2 to desensitize ferroptosis via E3 βTrCP, by which facilitates TFRC ubiquitiation and finally decreases labile iron in liver cancer cells.

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