Expression of Wild-Type and Variant Estrogen Receptor Alpha in Liver Carcinogenesis and Tumor Progression

Miceli, Vitale; Cocciadiferro, Letizia; Fregapane, Maria; Zarcone, Maurizio; Montalto, Giuseppe; Polito, Lucia M.; Agostara, Biagio; Granata, Orazia M.; Carruba, Giuseppe

doi:10.1089/omi.2010.0108

Cited by 53 publications

(50 citation statements)

References 8 publications

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“…There is some evidence that the membrane-initiated effects of E 2 and G-1 in breast cancer cells are not mediated by GPER but require ER␣36, a splice variant of ER␣ lacking exons 1, 7, and 8 and having an added unique 27-amino acid exon at the C terminus (36). ER␣36 was reported to be higher in HCC compared with normal or cirrhotic liver (62). We observed that DHEA and G-1 increased ER␣36 mRNA and protein in HepG2 cells.…”

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone Activation of G-protein-coupled Estrogen Receptor Rapidly Stimulates MicroRNA-21 Transcription in Human Hepatocellular Carcinoma Cells

Teng

Radde

Litchfield

et al. 2015

Journal of Biological Chemistry

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Background: is an oncomiR in human hepatocellular carcinoma and is highly expressed in liver, but its regulation is uncharacterized. Results: Dehydroepiandrosterone (DHEA) rapidly increases miR-21 transcription in HepG2 cells by activating G-proteincoupled estrogen receptor (GPER). Conclusion: miR-21 transcription is regulated by DHEA through GPER. Significance: GPER may be among the activators of miR-21 expression in human hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone Activation of G-protein-coupled Estrogen Receptor Rapidly Stimulates MicroRNA-21 Transcription in Human Hepatocellular Carcinoma Cells

Teng

Radde

Litchfield

et al. 2015

Journal of Biological Chemistry

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“…The latter did not mention which ERα antibody they used or which size of ERα bands they blotted (Liu et al, 2009). However, a recent study showed truncated but not full-length ESR1 mRNA was observed in human HCC tumors (Miceli et al, 2011). Thus, most of these studies have showed that ERα expression is lost or attenuated in human liver cancer cells and liver tumors, indicating the potential protective roles of estrogen signaling in human liver cancer and that defective estrogen signaling might lead to human liver cancer.…”

Section: Protective Roles Of Erα In Liver Cancermentioning

confidence: 99%

Interplay of estrogen receptors and FOXA factors in the liver cancer

Zhao

2015

Molecular and Cellular Endocrinology

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Liver cancer is the fifth most common cancer in human with male dominance. Sexual dimorphism of liver cancer is conserved from rodents to humans, which was firstly found in mice in late 1930s and female mice were resistant to liver cancer. Sex hormones were found to affect the incidence of liver cancer in rodents. Estrogen receptor alpha (ERα)-mediated estrogen signaling or androgen receptor-mediated androgen signaling prevents or promotes the growth of rodent liver tumors, respectively. Forkhead box protein A (Foxa) factors, Foxa1 and Foxa2, also known as pioneer transcription factors in liver specification, are essential for both estrogen and androgen signaling by acting as central regulators of sexual dimorphism in liver cancer. This review mainly focuses on the interplay between ERα and FOXA factors in liver cancer, and summarizes recent breakthrough studies in elucidating the mechanisms of sexual dimorphism in liver cancer.

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“…Accumulating evidence highlights the importance of ER-36-mediated non-genomic estrogen signaling in malignant growth of breast cancer and endometrial cancer cells. The expression of ER-36 has also been detected in other types of human cancer such as human colon cancer and liver cancer (Jiang et al, 2008;Miceli et al, 2011), suggesting that ER-36 may also involved in initiation and development of human malignancy in non-classical estrogen targeting organs. Elucidating the functions of ER-36-mediated non-genomic estrogen signaling in different types of human malignancy could provide more informed approaches to better understand the underlying mechanisms of mitogenic estrogen signaling in mammary carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

ER-Alpha36 Mediates Non-Genomic Estrogen and Anti-Estrogen Signaling in Breast Cancer Cells

Wang¹,

Zhang²,

Kang³

2011

Breast Cancer - Carcinogenesis, Cell Growth and Signalling Pathways

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Expression of Wild-Type and Variant Estrogen Receptor Alpha in Liver Carcinogenesis and Tumor Progression

Cited by 53 publications

References 8 publications

Dehydroepiandrosterone Activation of G-protein-coupled Estrogen Receptor Rapidly Stimulates MicroRNA-21 Transcription in Human Hepatocellular Carcinoma Cells

Dehydroepiandrosterone Activation of G-protein-coupled Estrogen Receptor Rapidly Stimulates MicroRNA-21 Transcription in Human Hepatocellular Carcinoma Cells

Interplay of estrogen receptors and FOXA factors in the liver cancer

ER-Alpha36 Mediates Non-Genomic Estrogen and Anti-Estrogen Signaling in Breast Cancer Cells

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