Aryl hydrocarbon receptor nuclear translocator is associated with tumor growth and progression of hepatocellular carcinoma

2011 ◽  
Vol 130 (8) ◽  
pp. 1745-1754 ◽  
Author(s):  
Ying Liang ◽  
Wei-Wei Li ◽  
Bi-Wei Yang ◽  
Zhong-Hua Tao ◽  
Hui-Chuan Sun ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon

scholarly journals The novel Aryl hydrocarbon receptor inhibitor biseugenol inhibits gastric tumor growth and peritoneal dissemination

Oncotarget ◽  
2014 ◽  
Vol 5 (17) ◽  
pp. 7788-7804 ◽  
Author(s):  
De-Wei Lai ◽  
Shing-Hwa Liu ◽  
Anna Isabella Karlsson ◽  
Wen-Jane Lee ◽  
Keh-Bin Wang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Aryl Hydrocarbon Receptor ◽  
Peritoneal Dissemination ◽  
Gastric Tumor ◽  
The Novel ◽  
Aryl Hydrocarbon ◽  
Receptor Inhibitor

scholarly journals A Protective Role of Aryl Hydrocarbon Receptor Repressor in Inflammation and Tumor Growth

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 589 ◽  
Author(s):  
Christoph F. A. Vogel ◽  
Yasuhiro Ishihara ◽  
Claire E. Campbell ◽  
Sarah Y. Kado ◽  
Aimy Nguyen-Chi ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Aryl Hydrocarbon Receptor ◽  
Inflammatory Responses ◽  
Environmental Pollutants ◽  
Protective Role ◽  
Potential Therapeutic Target ◽  
Embryonic Fibroblasts ◽  
Aryl Hydrocarbon ◽  
Enhancer Binding Protein

The aryl hydrocarbon receptor (AhR) is known for mediating the toxicity of environmental pollutants such as dioxins and numerous dioxin-like compounds, and is associated with the promotion of various malignancies, including lymphoma. The aryl hydrocarbon receptor repressor (AhRR), a ligand-independent, transcriptionally inactive AhR-like protein is known to repress AhR signaling through its ability to compete with the AhR for dimerization with the AhR nuclear translocator (ARNT). While AhRR effectively blocks AhR signaling, several aspects of the mechanism of AhRR’s functions are poorly understood, including suppression of inflammatory responses and its putative role as a tumor suppressor. In a transgenic mouse that overexpresses AhRR (AhRR Tg) we discovered that these mice suppress 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)- and inflammation-induced tumor growth after subcutaneous challenge of EL4 lymphoma cells. Using mouse embryonic fibroblasts (MEF) we found that AhRR overexpression suppresses the AhR-mediated anti-apoptotic response. The AhRR-mediated inhibition of apoptotic resistance was associated with a suppressed expression of interleukin (IL)-1β and cyclooxygenase (COX)-2, which was dependent on activation of protein kinase A (PKA) and the CAAT-enhancer-binding protein beta (C/EBPβ). These results provide mechanistic insights into the role of the AhRR to suppress inflammation and highlight the AhRR as a potential therapeutic target to suppress tumor growth.

scholarly journals Correction: Aryl hydrocarbon receptor regulates histone deacetylase 8 expression to repress tumor suppressive activity in hepatocellular carcinoma

Oncotarget ◽  
2018 ◽  
Vol 9 (102) ◽  
pp. 37807-37807
Author(s):  
Li-Ting Wang ◽  
Shyh-Shin Chiou ◽  
Chee-Yin Chai ◽  
Edward Hsi ◽  
Shen-Nien Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Aryl Hydrocarbon Receptor ◽  
Histone Deacetylase ◽  
Suppressive Activity ◽  
Aryl Hydrocarbon ◽  
Histone Deacetylase 8

scholarly journals Aryl hydrocarbon receptor regulates histone deacetylase 8 expression to repress tumor suppressive activity in hepatocellular carcinoma

Oncotarget ◽  
2016 ◽  
Vol 8 (5) ◽  
pp. 7489-7501 ◽  
Author(s):  
Li-Ting Wang ◽  
Shyh-Shin Chiou ◽  
Chee-Yin Chai ◽  
Edward Hsi ◽  
Shen-Nien Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Aryl Hydrocarbon Receptor ◽  
Histone Deacetylase ◽  
Suppressive Activity ◽  
Aryl Hydrocarbon ◽  
Histone Deacetylase 8

Carbidopa: a selective Ah receptor modulator (SAhRM)

2017 ◽  
Vol 474 (22) ◽  
pp. 3763-3765 ◽  
Author(s):  
Stephen Safe
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Aryl Hydrocarbon Receptor ◽  
Pancreatic Cancer Cell ◽  
Clinical Applications ◽  
Ah Receptor ◽  
High Affinity ◽  
Aryl Hydrocarbon ◽  
Receptor Modulator ◽  
Intracellular Receptor

The aryl hydrocarbon receptor (AhR) was discovered as the intracellular receptor that bound with high affinity to the environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and the AhR is required for mediating the toxicity induced by TCDD. Subsequent studies show that the AhR binds structurally diverse chemicals including plant-derived compounds that promote health and several AhR-active pharmaceuticals that exhibit anticancer activity. In this issue, there is a report that carbidopa, a drug used for treating Parkinson's disease, is also an AhR ligand, and this compound inhibits pancreatic cancer cell and tumor growth. These results are consistent with activities of other AhR-active compounds that inhibit carcinogenesis. Like carbidopa, these chemicals are selective AhR modulators with potential clinical applications that are AhR-dependent.

scholarly journals TDO2 Promotes the EMT of Hepatocellular Carcinoma Through Kyn-AhR Pathway

2021 ◽  
Vol 10 ◽  
Author(s):  
Lei Li ◽  
Tao Wang ◽  
Shanbao Li ◽  
Zhengqian Chen ◽  
Junyi Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Aryl Hydrocarbon ◽  
Hcc Cells

Tryptophan 2,3-dioxygenase (TDO2), an enzyme involved in tryptophan (Trp) metabolism has been linked with some malignant traits of various cancers. Kyn, the main product of Trp metabolism pathway catalyzed by TDO2 and indoleamine 2,3-dioxygenase (IDO) in tumor cells, was also demonstrated to activate aryl hydrocarbon receptor (AhR), which may regulate cancer growth and invasion in some malignancies. However, whether TDO2 participates in the metastasis and invasion of HCC has not been explored before. The underlying mechanism played by TDO2 in this process still requires further investigation. Here, we demonstrated that overexpression of TDO2 correlates with advanced stage or malignant traits in HCC patients. Knockdown or inhibition of TDO2 suppressed the migration and invasion of HCC cells in vitro and in vivo. Epithelial to mesenchymal transition (EMT) is an essential program happened in the initial phase of cancer metastasis. We found that in HCC cells, TDO2 promoted the EMT process evidenced by altered levels of biomarkers for EMT. Mechanically, TDO2 regulated the Kyn production in HCC cell via activated aryl hydrocarbon receptor (AhR). Together, these results indicate that TDO2 promotes the EMT of hepatocellular carcinoma through activating Kyn-AhR pathway, thereby participating in the metastasis and invasion of HCC.

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