ArticleCancer & metabolism2025
Obesity and cervical intraepithelial neoplasia: regulation of mitochondrial energy metabolism via the Kisspeptin/GPR54 signaling pathway.
Article in Cancer & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Obesityand Gynaecological Cancers, with a Focus on Morbid Obesity: Risk Stratification, Early Diagnosis and Management.Diagnostics (Basel, Switzerland) · 2026Review
- Investigation of Radiolabeled KISS1R Ligands as Promising Tools for Diagnosis and Treatment of Triple-Negative Breast Cancer.Molecular pharmaceutics · 2026Article
- Mitochondrial reprogramming in cervical cancer: crosstalk with tumor immunity, HPV oncogenic signaling, and therapeutic resistance.Frontiers in immunology · 2026Review
- Colorectal Adenocarcinoma: A Comprehensive Narrative Review of Molecular Pathogenesis, Metabolic Vulnerabilities, and Therapeutic Potential of Sorghum Polyphenols.Analytical cellular pathology (Amsterdam) · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundObesity exacerbates the severity of cervical intraepithelial neoplasia (CIN), potentially through metabolic alterations. This study investigates how the Kisspeptin/GPR54 signaling pathway mediates mitochondrial energy metabolism in obesity-related CIN.
methodsA clinical analysis of 980 samples was conducted to assess the correlation between Body Mass Index (BMI) and CIN grade. Transcriptomic analysis identified KISS1R as a key gene. Functional assays in cervical cancer (CC) cell lines, including CCK-8, wound healing, and Transwell assays, were used to evaluate the effects of KISS1 modulation. Mitochondrial function was assessed via oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) assays. A high-fat diet-induced CIN mouse model was used to investigate the in vivo effects.
resultsBMI positively correlated with CIN grade, with elevated KISS1R expression in higher CIN grades. Overexpression of KISS1 enhanced CC cell proliferation and migration by reprogramming mitochondrial energy metabolism. In high-fat environments, KISS1 silencing and mitochondrial activator PQQ modulated CC cell behavior. Activation of Kisspeptin/GPR54 in obese CIN mice exacerbated cervical lesions.
conclusionThe Kisspeptin/GPR54 signaling pathway enhances mitochondrial energy metabolism, promoting obesity-related CIN grade. These findings provide a potential molecular mechanism linking obesity to CC and suggest new therapeutic targets.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.