A novel therapeutic strategy for hepatocellular carcinoma: Immunomodulatory mechanisms of selenium and/or selenoproteins on a shift towards anti-cancer

2021 ◽  
Vol 96 ◽  
pp. 107790
Author(s):  
Bao-Kang Wu ◽  
Qian-Hui Chen ◽  
Dan Pan ◽  
Bing Chang ◽  
Li-Xuan Sang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Therapeutic Strategy ◽  
Anti Cancer ◽  
Novel Therapeutic

scholarly journals Prospects for immunotherapy as a novel therapeutic strategy against hepatocellular carcinoma

2019 ◽  
Vol 7 (3) ◽  
pp. 80-95
Author(s):  
Yu Akazawa ◽  
Toshihiro Suzuki ◽  
Toshiaki Yoshikawa ◽  
Shoichi Mizuno ◽  
Yasunari Nakamoto ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

Pharmacological inhibition of Axl tyrosine kinase as a novel therapeutic strategy in hepatocellular carcinoma.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. e15152-e15152 ◽  
Author(s):  
David James Pinato ◽  
Sebastian Trousil ◽  
Matthew Caley ◽  
Francesco A Mauri ◽  
Eric Aboagye ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tyrosine Kinase ◽  
Therapeutic Strategy ◽  
Pharmacological Inhibition ◽  
Novel Therapeutic

scholarly journals Cytotoxic Activity of Aplykurodin A Isolated From Aplysia kurodai against AXIN1-Mutated Hepatocellular Carcinoma Cells by Promoting Oncogenic β-Catenin Degradation

Marine Drugs ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 210
Author(s):  
Jaehoo Lee ◽  
Wei Zhou ◽  
MinKyun Na ◽  
Sangtaek Oh
Keyword(s):  
Hepatocellular Carcinoma ◽  
Therapeutic Strategy ◽  
Glycogen Synthase ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Human Hepatoma ◽  
Sensitive Cell ◽  
Novel Therapeutic ◽  
Stimulation Of

Dysregulation of the Wnt/β-catenin signaling pathway is involved in the development of human hepatocellular carcinoma and has thus emerged as a therapeutic target for this malignant tumor. In this study, we employed sensitive cell-based assays to identify aplykurodin A isolated from Aplysia kurodai as an antagonist of Wnt/β-catenin signaling. Aplykurodin A inhibited β-catenin responsive transcription, which was stimulated by a Wnt3a-conditioned medium or a glycogen synthase kinase 3β inhibitor by accelerating intracellular β-catenin degradation. Aplykurodin A downregulated the level of oncogenic β-catenin and decreased the expression of β-catenin-dependent gene, leading to inhibition of human hepatoma Hep3B and SNU475 cell proliferation. Moreover, apoptosis and autophagy were elicited by aplykurodin A, as indicated by an increase the number of Annexin V-FITC-stained cells and the formation of microtubule-associated protein 1 light chain 3 puncta, respectively, in Hep3B and SNU475 cells. Our findings suggest that aplykurodin A provides a novel therapeutic strategy for human hepatocellular carcinoma via stimulation of oncogenic β-catenin degradation.

Epithelial-to-Mesenchymal Transition (EMT) and Signal Transducers and Activators of Transcription (STAT3) Are a Novel Therapeutic Strategy for Hepatocellular Carcinoma (HCC) Prognosis

2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S134-S134
Author(s):  
Amira Fyala ◽  
Ahmed Sultan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Protein Expression ◽  
Cell Lines ◽  
Therapeutic Strategy ◽  
Epithelial To Mesenchymal Transition ◽  
Pivotal Role ◽  
Signal Transducers ◽  
Mesenchymal Transition ◽  
Novel Therapeutic ◽  
E Cadherin

Abstract Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide and is the second most common cancer in Egypt. Poor diagnosis of HCC is correlated with vascular invasion and metastasis. Epithelial-to-mesenchymal transition (EMT) is the main step in the tumor invasion process whereby epithelial cells lose cell polarity with each other and then undergo a dramatic remodeling of the cytoskeleton. Also, EMT plays a pivotal role in metastasis when epithelial cell layers lose cell-cell contacts in tumor progression due to the loss of E-cadherin and increasing the ability of the spread into surrounding tissues. Signal transducers and activators of transcription (STAT) play a different cellular function as signal transducers in the cytoplasm and transcription activators in the nucleus. STAT3 gene plays a crucial role to affect EMT in cancer progression by promoting cell proliferation and survival through its function as a transcription factor of the tumor. The aim of our study is to investigate the gene expression of STAT3 in HCC (HepG-2) cell lines and the expression of cell differentiation and proliferation markers. Western blotting was used to examine the protein expression of STAT3, E-cadherin, and β-catenin signaling. Our results showed that STAT3 expression levels were detected, as well as a significant increase in the expression of proliferation marker as β-catenin and a significant decrease of differentiation marker as E-cadherin protein expression levels in HepG-2 cell lines. Conclusion Our finding provides novel evidence for using a molecular gene therapy as STAT3, which showed an effect on EMT that plays a pivotal role in the prognosis of HCC. The loss of E-cadherin expression is a hallmark of EMT, because β-catenin is associated with the cytoplasmic domain of E-cadherin. We have emphasized the significant role of EMT and STAT3 in HCC progression, which could be a potential application as a novel therapeutic strategy for HCC treatment.

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