Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMedOpen access

A Novel Insight into the Role of Obesity-Related Adipokines in Ovarian Cancer-State-of-the-Art Review and Future Perspectives.

Kołakowska K., Kiśluk J., Nikliński J.

Narrative Review on Chronic Inflammation, published in Int J Mol Sci (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Int J Mol Sci (2025)
Country
Switzerland
Reported sample size
—
Source database
PubMed
PMID
40076482
PMCID
PMC11900017
DOI
10.3390/ijms26051857
Citations
4

Abstract (original English)

Ovarian cancer (OC) is one of the most fatal gynecological neoplasms. Meta-analyses have shown that the relationship between body mass index (BMI) and ovarian cancer incidence was detected in some types of ovarian cancer. Chronic inflammation and excessive accumulation of free fatty acids are key adipose tissue-derived factors initiating cancer development. Cancer cells transform adipose-derived stem cells into cancer-associated adipocytes, which produce adipokines and interleukins. It was revealed that adipokines exert a pleiotropic role in ovarian cancer pathogenesis. Chemerin presents both pro-cancer and anti-cancer action in ovarian cancer development. Chemerin induces angiogenesis and increases programmed death ligand-1 (PD-L1) expression, leading to enhanced proliferation and migration of OC cells. Apelin impacts cancer cell migration and acts as a mitogenic factor. Moreover, apelin exerts influence on lipid uptake into cancer cells and accelerates fatty acid oxidation, which provides energy for cancer cells. Visfatin induces matrix metallopeptidase 2 (MMP2) expression involved in extracellular matrix degradation and suppresses claudin 3 and 4 expression. Visfatin also induces a shift to anaerobic glucose metabolism and influences poly-ADP ribose polymerase (PARP). Resistin induces MMP2 and vascular endothelial growth factor (VEGF) expression and contributes to cisplatin-

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansOvarian NeoplasmsFemaleAdipokinesObesityAnimals

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