Autocrine Motility Factor Modulates Proliferation Signaling Mediated By GPER
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ABSTRACT:
PROVIDER: PRJNA471076 | ENA |
REPOSITORIES: ENA
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2019-03-12 | PXD009780 | Pride
Project description:Traditional surgery plus radiotherapy or chemotherapy, existing targeted therapies failed to significantly improve the survival rate of recurrent endometrial cancer, so suggesting that mechanism of recurrence and progression that modulates in endometrial cancer is clinically important. Here, we show that GPER(G protein-coupled estrogen receptor 1) was binded to AMF, and the complex were translocation form plasma to cytoplasmic. Mechanistic investigations elucidated that interaction of AMF with GPER triggers phosphoinositide-3-kinase (PI3K) signaling activating and accelerating the ability of endometrial cancer cells growth. Furthermore, we found that AMF may contribute to GPER-mediated endometrial cancer progression using animal experiments and human histological experiments which be consistent with the above conclusions. On the basis of these evidences including invivo and invitro, our findings suggest that AMF–GPER interaction might be novel key molecular targets for therapeutic management of patients with endometrial cancer, whose disease were progression and recurrence.
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Project description:Introduction: Type 1 diabetes (T1D) significantly affects gastrointestinal (GI) motility and contributes to complications, such as gastroparesis, constipation, and fecal incontinence. Notably, these complications have a higher prevalence in female patients, underscoring a critical knowledge gap in the understanding of the underlying mechanisms. Given the emerging role of the G-protein-coupled estrogen receptor (GPER) in GI motility regulation, our study investigated the potential contribution of diabetes-induced changes in GPER expression to pathophysiology. Hypothesis: We hypothesized that diabetes-induced perturbations in GPER expression contribute to pathophysiological mechanisms affecting GI motility in T1D, with notable sex-dependent variations. Methods: we assessed GPER mRNA and protein expression levels using quantitative reverse-transcription PCR and western blot analyses, and quantified the changes in nuclear DNA methyltransferases and histone modifications (H3K4Me3, H3Ac, and H3K27Ac) were quantified using ELISA kits. Targeted bisulfite and chromatin immunoprecipitation sequencing were used to evaluate DNA methylation and histone modifications around the GPER promoter by chromatin immunoprecipitation assays in gastric and colonic smooth muscle tissues of male and female control (CTR) and non-obese diabetic (NOD) mice. Results: Our results revealed significant downregulation of GPER in NOD mice, with marked sex-dependent variations. Mechanistically, this downregulation was associated with reduced H3K4me3, H3ac, and H3K27ac levels in NOD male gastric smooth muscle. In contrast, downregulation in female gastric smooth muscle cells has been linked to decreased H3K4me3 and H3ac levels. Male NOD colonic smooth muscle exhibited elevated H3ac and H3K27ac levels, whereas female NOD colonic smooth muscle demonstrated diminished enrichment of H3ac and H3K27ac at the GPER promoter. Additionally, DNA methylation is elevated in NOD male colonic smooth muscle compared to NOD females. Conclusion: Our findings elucidate sex-specific epigenetic mechanisms contributing to T1D-mediated suppression of GPER expression in the gastrointestinal tract. These insights not only advance our understanding of T1D complications but also suggest promising avenues for targeted therapeutic interventions.
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