The molecular mechanisms linking metabolic syndrome to endometrial and breast cancers

The metabolic syndrome represents a plethora of cardio-metabolic risk factors including obesity, arterial hypertension, atherogenic dyslipidemia, hyperglycemia, accompanied by pro-inflammatory and pro-thrombotic state. The metabolic syndrome is one of the key risk factors for certain types of cancer. Among these malignancies, breast cancer and endometrial neoplasms require special attention. Incriminated major causes for the development of breast and endometrial cancer in metabolic syndrome patients are: the pro-inflammatory status and related cytokines, adipokine imbalances, hyperestrogenism, growth factors, disturbances in cancer microenvironment, insulin resistance and hyperinsulinemia. The metabolic syndrome consists of molecular dysregulations that create a pro-oncogenic status. Our review aims at providing a better understanding of the mechanisms underlying the link between the metabolic syndrome and endometrial and breast cancer

MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis

Metabolic syndrome (MetS) represents a cluster of disorders that increase the risk of a plethora of conditions, in particular type two diabetes, cardiovascular diseases, and certain types of cancers. MetS is a complex entity characterized by a chronic inflammatory state that implies dysregulations of adipokins and proinflammatory cytokins together with hormonal and growth factors imbalances. Of great interest is the implication of microRNA (miRNA, miR), non-coding RNA, in cancer genesis, progression, and metastasis. The adipose tissue serves as an important source of miRs, which represent a novel class of adipokines, that play a crucial role in carcinogenesis. Altered miRs secretion in the adipose tissue, in the context of MetS, might explain their implication in the oncogenesis. The interplay between miRs expressed in adipose tissue, their dysregulation and cancer pathogenesis are still intriguing, taking into consideration the fact that miRNAs show both carcinogenic and tumor suppressor effects. The aim of our review was to discuss the latest publications concerning the implication of miRs dysregulation in MetS and their significance in tumoral signaling pathways. Furthermore, we emphasized the role of miRNAs as potential target therapies and their implication in cancer progression and metastasis

Diabetes and Obesity—Cumulative or Complementary Effects On Adipokines, Inflammation, and Insulin Resistance

Background: Diabetes and obesity are increasingly significant public health issues. The aim of this study was to evaluate the relationship between adipocytokines (leptin, ghrelin, and chemerin), inflammation (sVCAM1—soluble vascular adhesion molecule 1, sICAM1—soluble intercellular adhesion molecule 1), and insulin resistance in the presence of obesity and diabetes mellitus. Methods: 88 subjects, with a mean age of 61.96 ± 10.15 years, 75% of whom were women, were evaluated (in order to consider different associations between obesity and diabetes, subjects were categorized into four groups). Results: Overall, we found significant correlations between sICAM1-sVCAM1 rho = 0.426 and ghrelin-chemerin rho = −0.224. In the obesity + diabetes group, leptin correlated with sICAM1 rho = 0.786, and sVCAM1 negatively with glycemia/insulin rho = −0.85. Significant differences were found between the groups regarding sVCAM1 (p = 0.0134), leptin (p = 0.0265) and all insulin resistance scores, with differences influenced by the subjects’ gender. In conclusion, although there are currently many unknown aspects of the release and the role of various adipokines, in particular chemerin, its implication in early glucose metabolism dysregulation disorders seems very likely