The presence of plasma SHBG in HCC bearing mice suppressed the levels of steatosis and inflammation in a process mediated by estrogens and estrogen receptor alpha.
The susceptible FOXA1-Ala83 impairs its interaction with ERα, attenuates transactivation toward some of their dual target genes, such as DIO1, UGT2B17 and NTCP, but correlates with strengthened cellular expression of AFP and elevated AFP serum concentration in HCC patients (n = 1096).
In HCV-associated cirrhosis and HCC the decreased expression of estrogen receptor alfa (ERα) in male patients may explain the worse outcome of HCV infection in men than in women.
The physiological regulation of Oestrogen receptor α (ERα) and peroxisome proliferator-activated receptor alpha (PPARα) in Hepatocellular carcinoma (HCC) remains unknown.
The current editorial review critically analyses the study by Iyer et al (<i>WJG</i>, 2017) that investigated the expression of ER subtypes in liver samples collected from patients with a healthy liver, hepatitis C virus cirrhosis, and HCC.
To begin to understand the potential mechanisms of estrogens' inhibitory effects on HCC development, RNA sequencing was used to generate comprehensive global transcriptome profiles of the human HCC-derived HepG2 cell line following treatment of vehicle (control), estradiol (E2), estrogen receptor alpha- (ER<i>α</i>-) specific agonist 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT), or ER<i>β</i>-specific agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) using a small set of cells.
The roles of DEMs like hsa-mir-221 in HCC through interactions with DEGs such as ESR1 and CXCL12 may provide new clues for the diagnosis and treatment of HCC patients.
Taken together, our study identified two genetic variants at 6q25.1 newly associated with HCC risk, suggesting ESR1 and estrogen signaling may play a role in mediating susceptibility to HCC in Chinese population.
We observed significantly higher mRNA expression of ERα in HCV-related HCC liver tissues as compared to normals (<i>P</i> < 0.05) and ERβ in livers of HCV-related cirrhosis and HCV-related HCC subjects (<i>P</i> < 0.05).
Computational Discovery of Niclosamide Ethanolamine, a Repurposed Drug Candidate That Reduces Growth of Hepatocellular Carcinoma Cells In Vitro and in Mice by Inhibiting Cell Division Cycle 37 Signaling.
Our hypothesis is based on the fact that liver tissue express ER and its different variants exert multiple functions in various stages of liver disease and participate in an extremely complicated signal transduction process, therefore we believe that the presence of one or more SNPs of ESR1 and ESR2 genes may be related with the increase of risk in developing and the severity of HCC, as well as in the response to different treatments.
Our previous study identified that estrogen receptor alpha (ERα) protein is downregulated in 60% of female HCC cases, via a miR-18a elevation mediated suppression of ERα translation.
The aim of the present study was to investigate the effect of anti-estrogen treatment (fulvestrant) on the biological activity of hepatocellular carcinoma (HCC), involving the estrogen receptor α (ERα) and Wnt pathways, and to evaluate whether ERα and Wnt inhibitory factor-1 (WIF1) could be biomarkers for anti-estrogen clinical therapy.
Polymorphisms in estrogen receptor alpha (ESR1) are reported to be associated with the susceptibility to persistent HBV infection, HBV liver cirrhosis and HBV-related hepatocellular carcinoma (HCC).