Impact of obesity‑associated myeloid‑derived suppressor cells on cancer risk and progression (Review).
Carlos Jiménez-CorteganaCristian Gutiérrez-GarcíaFlora Sánchez-JiménezTeresa Vilariño-GarcíaRocio Flores-CamposAntonio Pérez-PérezCarmen GarnachoMaria L Sánchez-LeónDaniel J García-DomínguezLourdes Hontecillas-PrietoNatalia Palazón-CarriónLuis De La Cruz-MerinoVíctor Sánchez-MargaletPublished in: International journal of oncology (2024)
Obesity is a chronic disease caused by the accumulation of excessive adipose tissue. This disorder is characterized by chronic low‑grade inflammation, which promotes the release of proinflammatory mediators, including cytokines, chemokines and leptin. Simultaneously, chronic inflammation can predispose to cancer development, progression and metastasis. Proinflammatory molecules are involved in the recruitment of specific cell populations in the tumor microenvironment. These cell populations include myeloid‑derived suppressor cells (MDSCs), a heterogeneous, immature myeloid population with immunosuppressive abilities. Obesity‑associated MDSCs have been linked with tumor dissemination, progression and poor clinical outcomes. A comprehensive literature review was conducted to assess the impact of obesity‑associated MDSCs on cancer in both preclinical models and oncological patients with obesity. A secondary objective was to examine the key role that leptin, the most important proinflammatory mediator released by adipocytes, plays in MDSC‑driven immunosuppression Finally, an overview is provided of the different therapeutic approaches available to target MDSCs in the context of obesity‑related cancer.
Keyphrases
- insulin resistance
- metabolic syndrome
- weight loss
- high fat diet induced
- weight gain
- adipose tissue
- type diabetes
- low grade
- papillary thyroid
- induced apoptosis
- oxidative stress
- squamous cell
- high fat diet
- squamous cell carcinoma
- skeletal muscle
- stem cells
- high grade
- prostate cancer
- cell cycle arrest
- bone marrow
- signaling pathway
- mesenchymal stem cells
- cell death
- endoplasmic reticulum stress
- childhood cancer
- robot assisted
- rectal cancer