Advances in “adiponcosis”: Insights in the inner mechanisms at the base of adipose and tumour tissues interplay

Abstract

The epidemic spread of obesity is nowadays recognized as a global health and economic burden, arising great interest in the scientific community. The rate of adult obesity steadily increases concomitantly with the cancer incidence. As has been comprehensively reported, obesity is included among the multiple cancer risk factors and can progressively cause and/or exacerbate certain cancer types, as colorectal and breast cancers. The term adiponcosis was forged precisely to emphasize the interconnection between obesity and cancer onset and progression. The underlying mechanisms of adiponcosis have not been fully elucidated yet, may vary on cancer type, and depend on body fat distribution. It has been proposed that insulin resistance and related chronic hyperinsulinemia, increased insulin‐like growth factors production, chronic inflammation or increased bioavailability of steroid hormones could be responsible of cancer hallmarks. Additionally, it has been suggested that adipose tissue‐derived hormones, cytokines and adipokines, such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumorigenesis. This review summarizes the current evidence on pathways, hormones, cytokines and low‐chronic inflammation subtending adiponconsis, focusing on breast and colorectal cancers. In addition, we analyzed the lifestyle interventions that could attenuate the driving forces of obesity‐related cancer incidence and progression. Moreover, current targets and drugs, their pros and cons, as well as new mechanisms and targets with promising therapeutic potential in cancer are discussed. Depicting this complex interconnection will provide insights for establishing new therapeutic approaches to halt the obesity impacts and thwart cancer onset and progression.

miRNA levels are associated with body mass index in endometrial cancer and may have implications for therapy

“…Functional enrichment analysis predicted several GO molecular functions involved in obesity. For instance, calmodulin and calcium are involved in obesity, 40,41 insulin resistance, adipocytes differentiation, and metabolism 42,43 ; adiponectin, another predicted GO molecular functions, is a hormone and an adipokine protein that affects several metabolic functions, including insulin-sensitizing and anti-inflammatory effects. 44 All these data together highlight a potential link between these miRNAs and obesity, particularly in the case of miR-449a/449b targets, emphasizing the relationship between EC-body fatness.…”

The causal association between obesity and gastric cancer and shared molecular signatures: a large-scale Mendelian randomization and multi-omics analysis

“…Possible mechanisms linking obesity with gastric cancer encompass obesityassociated insulin resistance, abnormally elevated blood levels of insulin-like growth factor (IGF), and associated levels of adipokines such as adiponectin (APN), leptin, steroid hormones and cytokines. Each of these elements alters the nutritional milieu, potentially fostering an environment conducive to tumor initiation and progression (28).…”