Insulin resistance: an independent risk factor for lung cancer?

Petridou, Eleni; Sergentanis, Theodoros N.; Antonopoulos, Constantine N.; Dessypris, Nick; Matsoukis, Ioannis; Aronis, Konstantinos N.; Efremidis, Anna; Syrigos, Constantinos; Mantzoros, Christos S.

doi:10.1016/j.metabol.2010.12.002

Cited by 62 publications

(46 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Both approaches identified that MAPK, TLR, and renal cell carcinoma signaling pathways a as being important in smoking-induced lung cancer. In addition, purine and ether lipid metabolism; GnRH, ErbB, and insulin signaling; adherens junctions; regulation of autophagy; snare interaction in vesicular transport; and cell cycle were also found to play important roles (Table 4) [77–91], whereas six pathways (aminosugars metabolism, dentatorubropallidoluysian atrophy, melanoma, N-glycan biosynthesis, renal cell carcinoma, and glioma) were predicted here for the first time as being significant pathways in smoking-induced lung cancer.…”

Section: Discussionmentioning

confidence: 99%

In silico identification of potential key regulatory factors in smoking-induced lung cancer

et al. 2017

View full text Add to dashboard Cite

BackgroundLung cancer is a leading cause of cancer-related death worldwide and is the most commonly diagnosed cancer. Like other cancers, it is a complex and highly heterogeneous disease involving multiple signaling pathways. Identifying potential therapeutic targets is critical for the development of effective treatment strategies.MethodsWe used a systems biology approach to identify potential key regulatory factors in smoking-induced lung cancer. We first identified genes that were differentially expressed between smokers with normal lungs and those with cancerous lungs, then integrated these differentially expressed genes (DEGs) with data from a protein-protein interaction database to build a network model with functional modules for pathway analysis. We also carried out a gene set enrichment analysis of DEG lists using the Kinase Enrichment Analysis (KEA), Protein-Protein Interaction (PPI) hubs, and KEGG (Kyoto Encyclopedia of Genes and Genomes) databases.ResultsTwelve transcription factors were identified as having potential significance in lung cancer (CREB1, NUCKS1, HOXB4, MYCN, MYC, PHF8, TRIM28, WT1, CUX1, CRX, GABP, and TCF3); three of these (CRX, GABP, and TCF) have not been previously implicated in lung carcinogenesis. In addition, 11 kinases were found to be potentially related to lung cancer (MAPK1, IGF1R, RPS6KA1, ATR, MAPK14, MAPK3, MAPK4, MAPK8, PRKCZ, and INSR, and PRKAA1). However, PRKAA1 is reported here for the first time. MEPCE, CDK1, PRKCA, COPS5, GSK3B, BRCA1, EP300, and PIN1 were identified as potential hubs in lung cancer-associated signaling. In addition, we found 18 pathways that were potentially related to lung carcinogenesis, of which 12 (mitogen-activated protein kinase, gonadotropin-releasing hormone, Toll-like receptor, ErbB, and insulin signaling; purine and ether lipid metabolism; adherens junctions; regulation of autophagy; snare interactions in vesicular transport; and cell cycle) have been previously identified.ConclusionOur systems-based approach identified potential key molecules in lung carcinogenesis and provides a basis for investigations of tumor development as well as novel drug targets for lung cancer treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

In silico identification of potential key regulatory factors in smoking-induced lung cancer

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Despite inconsistent epidemiological evidence on the association of diabetes and lung cancer, it is biologically plausible that diabetes could increase the risk of lung cancer (33). Studies have shown that elevated insulin potentiates the activity of IGF-I either via direct upregulation or indirectly through the downregulation of IGF-binding protein 1 (34), which can lead to higher risk of lung cancer (35).…”

Section: Discussionmentioning

confidence: 99%

Diabetes and Lung Cancer Among Postmenopausal Women

et al. 2012

View full text Add to dashboard Cite

OBJECTIVEEpidemiological evidence of diabetes as a lung cancer risk factor is limited and conflicting. Therefore, we assessed associations among diabetes, diabetes therapy, and lung cancer risk in postmenopausal women participating in the Women’s Health Initiative (WHI) study.RESEARCH DESIGN AND METHODSPostmenopausal women (n = 145,765), ages 50–79 years, including 8,154 women with diabetes at study entry were followed for a mean of 11 years with 2,257 lung cancers diagnosed. Information on diabetes therapy was collected via two methods (self-reported information on treatment history collected on a questionnaire at baseline and a face-to-face review of current medication containers that participants brought to the baseline visit). Lung cancers were confirmed by central medical record and pathology report review. Cox proportional hazards regression models adjusted for lung cancer risk factors were used to estimate hazard ratios (HRs) (95% CI) for diagnosis of diabetes and treatment of disease as risk factors for lung cancer.RESULTSCompared with women without diabetes, women with self-reported treated diabetes had a significantly higher risk of lung cancer (HR 1.27 [95% CI 1.02–1.59]), with risks increasing for women with diabetes requiring insulin treatment (1.71 [1.15–2.53]). However, we did not observe a significant association between lung cancer risk and diabetes not treated with medication or with duration of diabetes.CONCLUSIONSPostmenopausal women with treated diabetes, especially those using insulin, have a significantly higher risk of lung cancer. The influence of diabetes severity and specific classes of therapy for diabetes on lung cancer risk require future study.

show abstract

“…Many studies have found no significant association between APN levels and lung cancer (LC) risk [141][142][143] . However, one study did find an increase in APN levels in LC patients compared to controls 144 .…”

Section: Lung Cancer (Lc)mentioning

confidence: 99%

Evolving role of adiponectin in cancer-controversies and update

Katira¹,

Tan²

2016

Cancer Biology &Amp; Medicine

View full text Add to dashboard Cite

Adiponectin (APN), an adipokine produced by adipocytes, has been shown to have a critical role in the pathogenesis of obesityassociated malignancies. Through its receptor interactions, APN may exert its anti-carcinogenic effects including regulating cell survival, apoptosis and metastasis via a plethora of signalling pathways. Despite the strong evidence supporting this notion, some work may indicate otherwise. Our review addresses all controversies critically. On the whole, hypoadiponectinaemia is associated with increased risk of several malignancies and poor prognosis. In addition, various genetic polymorphisms may predispose individuals to increased risk of obesity-associated malignancies. We also provide an updated summary on therapeutic interventions to increase APN levels that are of key interest in this field. To date efforts to manipulate APN levels have been promising, but much work remains to be done.

show abstract

Insulin resistance: an independent risk factor for lung cancer?

Cited by 62 publications

References 50 publications

In silico identification of potential key regulatory factors in smoking-induced lung cancer

In silico identification of potential key regulatory factors in smoking-induced lung cancer

Diabetes and Lung Cancer Among Postmenopausal Women

Evolving role of adiponectin in cancer-controversies and update

Contact Info

Product

Resources

About