A role for G-protein coupled estrogen receptor (GPER) in estrogen-induced carcinogenesis: Dysregulated glandular homeostasis, survival and metastasis

@article{Filardo2018ARF,
  title={A role for G-protein coupled estrogen receptor (GPER) in estrogen-induced carcinogenesis: Dysregulated glandular homeostasis, survival and metastasis},
  author={Edward J. Filardo},
  journal={The Journal of Steroid Biochemistry and Molecular Biology},
  year={2018},
  volume={176},
  pages={38-48}
}
  • E. Filardo
  • Published 1 February 2018
  • Biology, Medicine
  • The Journal of Steroid Biochemistry and Molecular Biology
View on Elsevier
doi.org
34 Citations
Highly Influential Citations
2
Background Citations
16
Methods Citations
1
Results Citations
1

34 Citations

Implications of estrogen and its receptors in colorectal carcinoma.

The most recent pre-clinical and experimental evidences related to ERs in CRC development are reported, and the actions of naturally occurring and synthetic compounds, which have a protective role against CRC development by acting as ER agonist are reviewed.

The G Protein-Coupled Estrogen Receptor (GPER) Expression Correlates with Pro-Metastatic Pathways in ER-Negative Breast Cancer: A Bioinformatics Analysis

Analysis of expression data of more than 2500 primary BC found that GPER levels are associated with pro-migratory and metastatic genes belonging to cell adhesion molecules (CAMs), extracellular matrix (ECM)-receptor interaction, and focal adhesion (FA) signaling pathways, which may pave the way to further dissect the network triggered by GPER in the breast malignancies lacking ER.

miR-338-3p Is Regulated by Estrogens through GPER in Breast Cancer Cells and Cancer-Associated Fibroblasts (CAFs)

Novel evidence is provided on the molecular mechanisms by which E2 may regulate miR-338-3p toward breast cancer progression and it is ascertained that miR -338- 3p positively correlates with overall survival in breast cancer patients, according to previous studies showing that miP-338 -3p may suppress the growth and invasion of different cancer cells.

GPER and Testicular Germ Cell Cancer

The implication of GPER/GPR30 in TGCCs pathophysiology and the arguments to consider GPER or GPR30 as a potential therapeutic target in humans are reviewed.

Activation of GPER suppresses the malignancy of osteosarcoma cells via down regulation of IL-6 and IL-8.

Downregulation of G Protein-Coupled Estrogen Receptor (GPER) is Associated with Reduced Prognosis in Patients with Gastric Cancer

Downregulation of GPER predicts poor prognosis in gastric cancer, suggesting GPER may act as a tumor suppressor through the regulation of EMT in Gastric cancer.

Autocrine motility factor promotes endometrial cancer progression by targeting GPER-1

Mechanistic investigations demonstrated that interaction between AMF and GPER-1 triggers phosphoinositide-3-kinase signaling and promotes EC cell growth and laid the foundation of targeting this pathway for treating endometrial cancer.

Therapeutic Perspectives on the Modulation of G-Protein Coupled Estrogen Receptor, GPER, Function

Current forms of estrogen therapy and the implications that GPER holds for these therapies are reviewed and existing GPER targeted drugs, additional approaches towards developing GPER-targeted therapies and how these therapies may complement existing modalities of estrogen- targeted therapy are discussed.

GPER1 Silencing Suppresses the Proliferation, Migration, and Invasion of Gastric Cancer Cells by Inhibiting PI3K/AKT–Mediated EMT

It is demonstrated that GPER1 inhibition suppresses the proliferation, migration, and invasion of gastric cancer cells by inhibiting PI3K/AKT-mediated EMT.

Environmental pollutants-dependent molecular pathways and carcinogenesis

This review focuses on recent research on environmental chemicals-driven molecular functions in human cancers, discussing the case of two receptors in mediating environmental pollutants effects: the established nuclear receptor, the Aryl hydrocarbon receptor (AhR) and the emerging membrane receptor, G-protein coupled estrogen receptor 1 (GPER1).

References

SHOWING 1-10 OF 152 REFERENCES

G Protein–Coupled Estrogen Receptor Regulates Mammary Tumorigenesis and Metastasis

This is the first description of a role for the novel estrogen receptor GPER in breast tumorigenesis and metastasis, demonstrating that it represents a new target in breast cancer diagnosis, prognosis, and therapy.

Estrogen regulates Hippo signaling via GPER in breast cancer.

The studies revealed that GPER stimulation activates yes-associated protein 1 (YAP) and transcriptional coactivator with a PDZ-binding domain (TAZ) and plays a critical role in breast tumorigenesis.

The novel estrogen receptor GPER regulates the migration and invasion of ovarian cancer cells

The data suggested that GPER promoted the migration and invasion of ovarian cancer cells by increasing the expression and activity of MMP-9, which might play an important role in the progression of ovariancancer.

Role of GPER on proliferation, migration and invasion in ligand‐independent manner in human ovarian cancer cell line SKOV3

It is established that GPER ligand‐independently stimulates the proliferation, migration and invasion of SKOV3 cells, which is a new aspect as a potential therapeutic strategy in ovarian cancer.

Estrogenic transmembrane receptor of GPR30 mediates invasion and carcinogenesis by endometrial cancer cell line RL95-2

The data suggest that, for the endometrial cancer cell line RL95-2, GPR30 plays important roles in mediating the proliferative and invasive effects of estrogen and in tumorigenesis.

G Protein-Coupled Estrogen Receptor-Selective Ligands Modulate Endometrial Tumor Growth

The results provide the first demonstration that pharmacological inhibition of GPER activity in vivo prevents estrogen-mediated tumor growth and have important implications with respect to the use of putatively ER-selective ligands and particularly for the widespread long-term use of “ER-targeted” therapeutics.

Multiple direct and indirect mechanisms drive estrogen-induced tumor growth in high grade serous ovarian cancers

Novel insights are described into the impact of E2 on tumor microenvironment, independently of its direct effect on tumor cell growth, thus supporting the idea that multiple direct and indirect mechanisms drive estrogen-induced tumor growth in HGSOC.

Genotoxic metabolites of estradiol in breast: potential mechanism of estradiol induced carcinogenesis

GPER functions as a tumor suppressor in triple-negative breast cancer cells

The results establish the protective role in breast cancer tumorigenesis, and the cell surface expression of GPER makes it an excellent potential therapeutic target for triple-negative breast cancer.

TFAP2C controls hormone response in breast cancer cells through multiple pathways of estrogen signaling.

TFAP2C is a central control gene of hormone response and is a novel therapeutic target in the design of new drug treatments for breast cancer.
...