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.
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.
The expression of MTA1 in hepatocellular carcinoma (HCC) and its potential relationship to metastasis and to estrogen receptor alpha (ER-alpha) expression has not been examined, forming the basis for this study.
The physiological regulation of Oestrogen receptor α (ERα) and peroxisome proliferator-activated receptor alpha (PPARα) in Hepatocellular carcinoma (HCC) remains unknown.
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 purpose of this study was to investigate whether miR-26a, regulated by a human α-fetoprotein (hAFP) and human telomerase reverse transcriptase (hTERT) dual promoter, could be specifically expressed in liver tumor cells to suppress their growth and to clarify whether estrogen receptor-α (ERα) is regulated by miR-26a and involved in the HCC process.
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.
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).
This was due to a decreased mRNA expression of estrogen receptor alpha (ESR1) and a reduced activation of NF-kappaB, which both are implicated in the development of 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.
To investigate whether arsenic exposure in utero causes altered estrogen signaling, we examined expression of estrogen receptor-alpha (ER-alpha), cyclin D1 (an estrogen-responsive hepatic oncogene), and several cytochrome P450 genes (with sexually dimorphic liver expression patterns) in livers from adult male mice with in utero arsenic-induced HCC.
Variant estrogen receptor transcripts (lacking exon 5 of the hormone binding domain) were investigated by reverse transcription-PCR in 14 patients (7 males and 7 females) with HCC.
We also show that transcriptional activity of reporter constructs containing human angiotensinogen gene promoter with nucleoside A at -20 is increased on cotransfection of an expression vector containing human estrogen receptor-alpha coding sequence in human hepatoma cells (HepG2) followed by estrogen treatment.
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).