The peroxisome proliferator-activated receptors (PPARs) belong to the ligand-inducible nuclear hormone receptor superfamily including three major members: PPARα (also called NR1C1), PPARβ/δ (also called NR1C2), and PPARγ (also called NR1C3). Despite several similarities, each PPAR isoform shows specific functions likely due to different biochemical properties, variable tissue distribution, and differential responses to different ligands. PPAR transcriptional activity can be modulated through a nongenomic cross-talk with phosphatases and kinases, including ERK1/2, p38-MAPK, PKA, PKC, AMPK, and GSK3. PPARs can form heterodimers with retinoid X receptor (RXR) modulating the expression of genes involved in lipid metabolism, adipogenesis, maintenance of metabolic homeostasis, and inflammation and inducing also anticancer effects in a variety of human tumors. Although all PPAR isoforms are implicated in several metabolic syndromes, PPARγ seems to be mostly involved in tumorigenesis regulation via activation of different pathways. Therefore, the modulation of PPAR signaling pathways could be a potential novel strategy to inhibit carcinogenesis and tumor progression. PPARγ can be activated by natural ligands, such as fatty acids and their derivatives, as well as synthetic ligands, such as thiazolidinediones (TZDs), including ciglitazone, rosiglitazone, troglitazone, and pioglitazone.

TZDs have been shown to be a class of drugs with potent insulin-sensitizing activity used to improve lipid and glucose metabolism in obesity and type 2 diabetes via PPAR. Since accumulating evidence highlighted the role of PPAR signaling in carcinogenesis, type 2 diabetes, and other metabolic disorders, such as obesity, understanding the potential molecular mechanisms underlying the interplay between metabolism, PPAR signaling, and cancer may represent an interesting research field for the development of novel strategies useful for the prevention and treatment of cancer. Since there exists a strong correlation between obesity and diabetes and both have been also shown to increase the cancer risk, the identification of the molecular mechanisms by which PPAR modulates these events may help us to better understand how the diet may affect the cancer susceptibility.

We invite investigators to submit original research articles as well as review articles that aim to increase our knowledge about the correlation between metabolic syndromes and cancer via activation of different PPAR signaling pathways in order to identify novel potential therapeutic targets involved in the development of cancer and cancer-related metabolic syndromes.

Potential topics include but are not limited to the following:

• Involvement of PPAR signaling pathway in carcinogenesis
• PPARs and cancer stem cells
• PPAR ligands as therapeutic agents in several types of cancers
• Toxicity associated with the exposure to PPAR ligands
• Nongenomic events induced by PPAR ligands
• Role of PPARs in different cancer-related metabolic syndromes
• Role of PPARs in modulating the cancer risk induced by diabetes and obesity