GPER1 (G Protein-Coupled Estrogen Receptor 1)

Our results suggest that the surface chemistry of silver nanoparticles may facilitate their ability to modulate estrogen signaling and interact with the estrogen receptor. Furthermore, the nanoplastics pollution may influence the cytotoxicity of silver nanoparticles. This paper highlights the importance of endocrine research in breast cancer, particularly within the context of nanoplastics pollution and the use of nanotechnology in breast cancer treatment.

In conclusion, the expression of GPER1 is reduced in EC. Overexpression of GPER1 enhances ferroptosis in EC, primarily through activation of the cAMP signaling pathway.

Conclusion GPER1 modulates macrophage M2 polarization through the MYC-IL-10 axis, thereby affecting gastric cancer progression. These findings indicate GPER1 as a potential therapeutic target for gastric cancer intervention.

In this review, we synthesize mechanistic and clinical evidence across lung diseases; delineate areas where data remain incomplete or contradictory; and outline opportunities for experimental and translational innovation. These include development of receptor-selective or biased ligands, inhaled or localized delivery, and implementation of sex-aware clinical trial designs to leverage estrogen-receptor biology for precision respiratory therapeutics.

Recruited to centrosomes by AKAP450, PKA phosphorylates Centrin-2, predominantly at aberrant centrioles and unexpectedly even outside of mitosis. These findings reveal a GPER1-PKA-Centrin signaling axis in CRC cells that regulates centrosome numbers and centriole integrity, shedding light on centrosome abnormalities that drive neoplastic transformation and tumor progression.

In conclusion, we postulate that AOH has pro-oxidative ability and that this effect is partially mediated by GPER1. Moreover, we postulated that HIF1α/PI3K/Akt and CLDNs participate in AOH action in OC cells, which in turn provides useful information for future toxicological research studies as a new molecular mechanism of AOH.

The molecular mechanisms of these non-genomic functions involve signal transduction via focal activated kinase (FAK), mitogen-activated protein kinase (ERK1/2), and phosphatidylinositol 3-kinase (PI3K), as well as the differential expression of multiple genes associated with various cellular processes. As a hormone receptor, integrin αvβ3, collaborating with ER-α and GPER, exhibits a wide range of cellular effects relevant to cancer biology.

NM-105 caused hypermethylation, unlike the other TiO2NPs. This study highlights DNA methylation relevance in assessing NMs' toxicity.

Similarly to daidzein, G-1 upregulated the expression of GPER1 forms, but down-regulated ERK and AKT phosphorylation. These results demonstrate the functional complexity of GPER1 signalling through different agonists and that daidzein modulates the expression of multiple GPER1 forms in TNBC cells in a GPER1-dependent manner, suggesting a potential therapeutic application for this phytoestrogen in non-classical estrogen signaling.

BMP1 appears to be involved in GPER1-mediated progression of luminal A breast cancer cells. In addition, BMP1 may play a role in tamoxifen-resistance.

This framework invites translational trials using biomarker-enriched patient stratification. If validated, it could reshape the role of sex hormones in male psychiatry-not as contraindications, but as precision neuromodulators aligned with neurobiological pathology.

In particular, G-1 induced CSE expression and increased H2S production in human endothelial EA.hy926 cells, inhibited tumor necrosis factor-alpha (TNF-α)-induced expression of nuclear factor kappa B (NF-kB), and decreased the expression of intracellular adhesion molecules. These findings confirm that GPER affects H2S production by regulating CSE expression through novel signaling mechanisms, which could be utilized as a potential therapeutic target to prevent endothelial dysfunction in cardiovascular disease.