scholarly journals ERα down‐regulates carbohydrate responsive element binding protein and decreases aerobic glycolysis in liver cancer cells

2021 ◽  
Author(s):  
Ying Lu ◽  
Na Tian ◽  
Lei Hu ◽  
Jian Meng ◽  
Ming Feng ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Aerobic Glycolysis ◽  
Liver Cancer Cells ◽  
Element Binding Protein ◽  
Responsive Element

scholarly journals ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Hui Du ◽  
Yun Le ◽  
Fenyong Sun ◽  
Kai Li ◽  
Yanfeng Xu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Liver Cancer Cells ◽  
Binding Factor ◽  
Element Binding Protein

Cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) is overexpressed and has an oncogenic role in hepatocellular carcinoma (HCC). Interleukin enhancer binding factor 2 (ILF2) has become research hotspot in liver cancer recently. However, it is still unclear whether and how CREB and ILF2 interact with each other. And how this interaction exerts its role in occurrence and development of liver cancer is still unclear. Here, we found that ILF2 directly bound with CREB, and this binding was essential for the malignant phenotypes of liver cancer cells. Moreover, we found that ILF2 acted as one of the upstream proteins of CREB and promoted CREB only in the protein level, whereas ILF2 expression was not regulated by CREB. Mechanistically, ILF2 bound to the pKID domain of CREB and stimulated its phosphorylation at Ser133. Taken together, our study finds a novel interaction between CREB and ILF2 in liver cancer, and this interaction might play a role in the diagnosis and remedy of liver cancer.

scholarly journals Metformin Resensitizes Sorafenib-Resistant HCC Cells Through AMPK-Dependent Autophagy Activation

2021 ◽  
Vol 8 ◽  
Author(s):  
Hong-Yue Lai ◽  
Hsin-Hwa Tsai ◽  
Chia-Jui Yen ◽  
Liang-Yi Hung ◽  
Ching-Chieh Yang ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Cohort Analysis ◽  
Growth Factor Receptor ◽  
Study Cohort ◽  
Primary Resistance ◽  
Liver Cancer Cells ◽  
Egfr Expression

Despite the activation of autophagy may enable residual cancer cells to survive and allow tumor relapse, excessive activation of autophagy may eventually lead to cell death. However, the details of the association of autophagy with primary resistance in hepatocellular carcinoma (HCC) remain less clear. In this study, cohort analysis revealed that HCC patients receiving sorafenib with HBV had higher mortality risk. We found that high epidermal growth factor receptor (EGFR) expression and activity may be linked to HBV-induced sorafenib resistance. We further found that the resistance of EGFR-overexpressed liver cancer cells to sorafenib is associated with low activity of AMP-activated protein kinase (AMPK) and CCAAT/enhancer binding protein delta (CEBPD) as well as insufficient autophagic activation. In response to metformin, the AMPK/cAMP-response element binding protein (CREB) pathway contributes to CEBPD activation, which promotes autophagic cell death. Moreover, treatment with metformin can increase sorafenib sensitivity through AMPK activation in EGFR-overexpressed liver cancer cells. This study suggests that AMPK/CEBPD-activated autophagy could be a potent strategy for improving the efficacy of sorafenib in HCC patients.

scholarly journals Ras responsive element binding protein-1 (RREB-1) down-regulates hZIP1 expression in prostate cancer cells

The Prostate ◽  
2009 ◽  
Vol 70 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Beatrice C. Milon ◽  
Anthony Agyapong ◽  
Roderick Bautista ◽  
Leslie C. Costello ◽  
Renty B. Franklin
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Prostate Cancer Cells ◽  
Element Binding Protein ◽  
Responsive Element

MicroRNA-64 Promotes Progression of Liver Cancer Through Targeting X-Box Binding Protein 1 (XBP1)

2021 ◽  
Vol 11 (8) ◽  
pp. 1555-1559
Author(s):  
Haiying Jiang ◽  
Jieming Yi ◽  
Shouren Cheng
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Binding Protein ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Liver Cancer Cells ◽  
Potential Binding ◽  
Gene Assay ◽  
Insight Into

Liver cancer is still a horrible threat to people’s health worldwide. Herein, we aimed to explore the mechanism underlying microRNA (miR)-64’s role in liver cancer progression to provide novel insight into therapy. Expression of miR-64 in liver cancer cells was determined by RT-qPCR. Luciferase reporter gene assay detected the potential binding between miR-64 and X-box binding protein 1 (XBP1). Cancer cells were transfected with specific plasmids of XBP1, followed by MTT experiment and Ttranswell assay to assess invasion and proliferation. miR-64 was highly expressed in liver cancer cells and positively correlated with cell proliferation, invasion, and metastasis. miR-64 targeted and inhibited XBP1 expression. Overexpression of miR-64 significantly resulted in increased cell viability and invasion. Taken altogether, miR-64 promotes liver cancer through inhibiting XBP1, providing insight into miR-64-based targeted therapy against liver cancer.

scholarly journals Metformin Resensitizes Sorafenib-Resistant HCC Cells Through AMPK-Dependent Autophagy Activation

2021 ◽  
Vol 8 ◽  
Author(s):  
Hong-Yue Lai ◽  
Hsin-Hwa Tsai ◽  
Chia-Jui Yen ◽  
Liang-Yi Hung ◽  
Ching-Chieh Yang ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Cohort Analysis ◽  
Growth Factor Receptor ◽  
Study Cohort ◽  
Primary Resistance ◽  
Liver Cancer Cells ◽  
Egfr Expression

Despite the activation of autophagy may enable residual cancer cells to survive and allow tumor relapse, excessive activation of autophagy may eventually lead to cell death. However, the details of the association of autophagy with primary resistance in hepatocellular carcinoma (HCC) remain less clear. In this study, cohort analysis revealed that HCC patients receiving sorafenib with HBV had higher mortality risk. We found that high epidermal growth factor receptor (EGFR) expression and activity may be linked to HBV-induced sorafenib resistance. We further found that the resistance of EGFR-overexpressed liver cancer cells to sorafenib is associated with low activity of AMP-activated protein kinase (AMPK) and CCAAT/enhancer binding protein delta (CEBPD) as well as insufficient autophagic activation. In response to metformin, the AMPK/cAMP-response element binding protein (CREB) pathway contributes to CEBPD activation, which promotes autophagic cell death. Moreover, treatment with metformin can increase sorafenib sensitivity through AMPK activation in EGFR-overexpressed liver cancer cells. This study suggests that AMPK/CEBPD-activated autophagy could be a potent strategy for improving the efficacy of sorafenib in HCC patients.

Multipurpose efficacy of ZnO nanoparticles coated by the crustacean immune molecule β-1, 3-glucan binding protein: Toxicity on HepG2 liver cancer cells and bacterial pathogens

2017 ◽  
Vol 158 ◽  
pp. 257-269 ◽  
Author(s):  
Arokiadhas Iswarya ◽  
Baskaralingam Vaseeharan ◽  
Mahalingam Anjugam ◽  
Balasubramaniem Ashokkumar ◽  
Marimuthu Govindarajan ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Zno Nanoparticles ◽  
Binding Protein ◽  
Bacterial Pathogens ◽  
Liver Cancer Cells ◽  
Immune Molecule ◽  
Protein Toxicity

Panobinostat treatment determines oncogenic miRNAs down-regulation in liver cancer cells

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
A Henrici ◽  
R Montalbano ◽  
K Quint ◽  
M Ocker ◽  
P Di Fazio
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Down Regulation ◽  
Liver Cancer Cells ◽  
Oncogenic Mirnas
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