scholarly journals Inhibition of AMPK activity by TRIM11 facilitates cell survival of hepatocellular carcinoma under metabolic stress

2021 ◽  
Vol 11 (12) ◽  
Author(s):  
Yanfeng Liu ◽  
Yingying Xu ◽  
Fan Wang ◽  
Yu Tong ◽  
Hongchang Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Survival ◽  
Metabolic Stress ◽  
Ampk Activity

scholarly journals Intermedin facilitates hepatocellular carcinoma cell survival and invasion via ERK1/2-EGR1/DDIT3 signaling cascade

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Fei Xiao ◽  
Hongyu Li ◽  
Zhongxue Feng ◽  
Luping Huang ◽  
Lingmiao Kong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Er Stress ◽  
Cell Survival ◽  
Vascular Remodeling ◽  
Therapeutic Potential ◽  
Blood Perfusion ◽  
Signaling Cascade ◽  
Apoptotic Pathway ◽  
High Level ◽  
Hcc Cells

AbstractAs one of the most malignant cancer types, hepatocellular carcinoma (HCC) is highly invasive and capable of metastasizing to distant organs. Intermedin (IMD), an endogenous peptide belonging to the calcitonin family, has been suggested playing important roles in cancer cell survival and invasion, including in HCC. However, how IMD affects the behavior of HCC cells and the underlying mechanisms have not been fully elucidated. Here, we show that IMD maintains an important homeostatic state by activating the ERK1/2-EGR1 (early growth response 1) signaling cascade, through which HCC cells acquire a highly invasive ability via significantly enhanced filopodia formation. The inhibition of IMD blocks the phosphorylation of ERK1/2, resulting in EGR1 downregulation and endoplasmic reticulum stress (ER) stress, which is evidenced by the upregulation of ER stress marker DDIT3 (DNA damage-inducible transcript 3). The high level of DDIT3 induces HCC cells into an ER-stress related apoptotic pathway. Along with our previous finding that IMD plays critical roles in the vascular remodeling process that improves tumor blood perfusion, IMD may facilitate the acquisition of increased invasive abilities and a survival benefit by HCC cells, and it is easier for HCC cells to obtain blood supply via the vascular remodeling activities of IMD. According to these results, blockade of IMD activity may have therapeutic potential in the treatment of HCC.

scholarly journals Carnitine palmitoyltransferase 1C promotes cell survival and tumor growth under conditions of metabolic stress

2011 ◽  
Vol 25 (10) ◽  
pp. 1041-1051 ◽  
Author(s):  
K. Zaugg ◽  
Y. Yao ◽  
P. T. Reilly ◽  
K. Kannan ◽  
R. Kiarash ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cell Survival ◽  
Metabolic Stress ◽  
Carnitine Palmitoyltransferase

Up-regulation of the fibroblast growth factor 8 subfamily in human hepatocellular carcinoma for cell survival and neoangiogenesis

Hepatology ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 854-864 ◽  
Author(s):  
Christine Gauglhofer ◽  
Sandra Sagmeister ◽  
Waltraud Schrottmaier ◽  
Carina Fischer ◽  
Chantal Rodgarkia-Dara ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Cell Survival ◽  
Fibroblast Growth Factor ◽  
Human Hepatocellular Carcinoma ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8

scholarly journals TRIM25 promotes the cell survival and growth of hepatocellular carcinoma through targeting Keap1-Nrf2 pathway

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yanfeng Liu ◽  
Shishi Tao ◽  
Lijuan Liao ◽  
Yang Li ◽  
Hongchang Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Survival ◽  
Nrf2 Pathway ◽  
Survival And Growth

scholarly journals The Role of ZNF143 in Breast Cancer Cell Survival Through the NAD(P)H Quinone Dehydrogenase 1–p53–Beclin1 Axis Under Metabolic Stress

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 296 ◽  
Author(s):  
A Paek ◽  
Ji Mun ◽  
Mun Jo ◽  
Hyosun Choi ◽  
Yun Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Zinc Finger Protein ◽  
Metabolic Stress ◽  
Cancer Cell Survival ◽  
Autophagic Process ◽  
Low Expression

Autophagy is a cellular process that disrupts and uses unnecessary or malfunctioning components for cellular homeostasis. Evidence has shown a role for autophagy in tumor cell survival, but the molecular determinants that define sensitivity against autophagic regulation in cancers are not clear. Importantly, we found that breast cancer cells with low expression levels of a zinc-finger protein, ZNF143 (MCF7 sh-ZNF143), showed better survival than control cells (MCF7 sh-Control) under starvation, which was compromised with chloroquine, an autophagy inhibitor. In addition, there were more autophagic vesicles in MCF7 sh-ZNF143 cells than in MCF7 sh-Control cells, and proteins related with the autophagic process, such as Beclin1, p62, and ATGs, were altered in cells with less ZNF143. ZNF143 knockdown affected the stability of p53, which showed a dependence on MG132, a proteasome inhibitor. Data from proteome profiling in breast cancer cells with less ZNF143 suggest a role of NAD(P)H quinone dehydrogenase 1(NQO1) for p53 stability. Taken together, we showed that a subset of breast cancer cells with low expression of ZNF143 might exhibit better survival via an autophagic process by regulating the p53–Beclin1 axis, corroborating the necessity of blocking autophagy for the best therapy.

scholarly journals Targeting the metabolic stress response in hepatocellular carcinoma to potentiate TACE-induced ischemia

2015 ◽  
Vol 26 (2) ◽  
pp. S17
Author(s):  
T.P. Gade ◽  
E. Tucker ◽  
S. Hunt ◽  
M. Nakazawa ◽  
B. Krock ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stress Response ◽  
Metabolic Stress
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