GPER1 (G Protein-Coupled Estrogen Receptor 1)

Tissue microarray validation (n = 167) confirmed high ATF5 expression predicts improved recurrence-free survival specifically in female patients (HR = 0.34, p = 0.040) but not males (p = 0.080). The ATF5-GPER1 axis represents a female-protective circuit operating through tumor-intrinsic suppression and immune remodeling, offering mechanistic insight into HCC sexual dimorphism and identifying ATF5 as a sex-specific prognostic biomarker with potential therapeutic implications.

Conclusion, this study suggested that the estrogen-like endocrine-disrupting response induced by metamifop, potentially mediated via non-classical estrogen signaling pathways (e.g., GPER1-KMT2D axis), rather than direct ERα activation. These findings provide scientific evidence for assessing metamifop endocrine-disrupting effects and environmental risks.

Furthermore, E4 modulated the expression of key mitochondrial genes, specifically upregulating the phosphate carrier SLC25A23 while downregulating the complex I subunit NDUFA1. In conclusion, E4 improves mitochondrial health and supports neuronal integrity via a multi-receptor mechanism, highlighting its potential as a safe neuroprotective therapy for AD.

This review synthesizes current knowledge while highlighting areas requiring further investigation. Evaluation of the urinary bladder for calcification and malignancy is advised when PG is detected, to explore potential associations for future research.

Notably, GPR30 inhibition attenuated MEHP-induced promotion of MCF-7 cell proliferation and migration through modulating of EMT process.

In endometrial cancer, estrogen signaling shifts from hormone-dependent initiation to progressive oncogenic autonomy through receptor rewiring and non-genomic pathways. By integrating these mechanisms, this review highlights estrogen receptor plasticity as a unifying concept across gynecological malignancies and outlines key knowledge gaps that are relevant for future endocrine strategies.

Moreover, HO-AAVPA reduced the activation and activity of CAFs. Our results support the notion that HDAC1 inhibition may be a novel approach to sensitizing resistant tumor cells to chemotherapy and radiotherapy by increasing GPER1 expression, and thus the use of antiproliferative GPER1 agonists/antagonists, at least in the early stages, without causing significant changes in liver function or morphological alterations.

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.