Abstract
Alterations of adipose tissue occurring in obesity have been recognized as a major risk factor for several cancers. The relationship between adipose tissue and lung cancer, which is the main cancer-related cause of death worldwide, still requires investigation. Perturbations in the adipokine system are likely to interfere with inter-organ crosstalk in lung cancer, which may influence the lung tumor microenvironment. Adiponectin (Acrp30) expression is deregulated in several cancer types. Acrp30 circulates as oligomers with a Low (LMW), Medium (MMW), and High Molecular Weight (HMW), with the latter mediating the main biological effects. Acrp30 acts through AdipoR1 and AdipoR2 receptors. T-cadherin has been described as a non-signaling receptor. This study’s aim was to investigate the regulation of serum Acrp30 and its receptors in sample tissue from non-small cell lung cancer (NSCLC) patients. We recruited 72 NSCLC patients and 60 healthy controls, whom we evaluated in terms of their Acpr30 levels and oligomeric profile. In addition, the expression of AdipoRs in tissues from lung cancer specimens was also measured and compared to coupled healthy lung samples. Our findings show a significant reduction of total Acrp30 levels in NSCLC patients compared to normal subjects, with a specific down-regulation of HMW oligomers. Acrp30 expression was lower in lung adenocarcinoma than other subtypes, regardless of other factors. A significantly higher expression of AdipoR1 was observed, while no differences in R2 and a lower expression of T-cadherin were found in lung cancer specimens compared to normal healthy lung tissues. Involvement of the Acrp30 system in lung cancer may provide new insight into the interaction between adipose tissue and lung and sheds light on its potential ability to influence the lung tumor microenvironment.
Highlights
Lung cancer is the main cancer-related cause of death in developed countries, with an unsatisfactory five-year survival rate, ranging from 10 to 15% [1,2]
The fasting glucose, alanine transaminase (ALT), aspartate transaminase (AST), and gamma glutamyl transferase (GGT) levels were significantly higher among non-small cell lung cancer (NSCLC) patients compared to among controls
Lower Acpr30 levels were documented in adenocarcinoma patients (n = 30, median 9.5 μg/mL (QR 8–10.7)) than in NSCLC with other subtypes (n = 40, median 12.4 μg/mL (IQR 10.5–14.6))
Summary
Lung cancer is the main cancer-related cause of death in developed countries, with an unsatisfactory five-year survival rate, ranging from 10 to 15% [1,2]. Despite substantial advances in our understanding of the molecular basis of lung cancer [4,5,6,7,8,9], ongoing research on driver genes, mechanisms of immune evasion, and the tumor microenvironment, which triggers crosstalk phenomena between organs/tissues, is expected to improve both early disease detection and survival [10]. The molecular and cellular mechanisms by which adipose tissue affects both tumor initiation and progression have not yet been completely elucidated. It is well-known that, beyond the adipose tissue volume, the presence of either inflammation/adipocyte hypertrophy or hypoxia reflects the metabolic and inflammatory status involved in the disruption of local and systemic physiological body homeostasis [15]. Adipocytes, through the production and secretion of different adipokines, while facilitating inter-organ crosstalk, indirectly affect the biology of tumor cells by regulating insulin resistance and inflammation [16,17]
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