Variations of chromosome 2 gene expressions among patients with lung cancer or non-cancer

Bao, Lianmin; Zhang, Yong; Wang, Jian; Wang, Haiyun; Dong, Nian; Su, Xiaojie; Xu, Menglin; Wang, Xiangdong

doi:10.1007/s10565-016-9343-z

Cited by 50 publications

(29 citation statements)

References 47 publications

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“…Several studies have linked CORVET, CHEVI and HOPS subunits to cancer progression. High levels of Vps3 correlate with poor prognosis of human squamous carcinoma lung cancer (Bao et al, 2016). Single nucleotide polymorphisms in Vps41 strongly associate with hereditary melanoma (Ibarrola-Villava et al, 2015), and a recent study reported Vps33B as an important tumor suppressor in hepatocarcinogenesis (Wang et al, 2018).…”

Section: Cancermentioning

confidence: 99%

CORVET, CHEVI and HOPS – multisubunit tethers of the endo-lysosomal system in health and disease

Beek

Jonker

Welle

et al. 2019

Journal of Cell Science

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Multisubunit tethering complexes (MTCs) are multitasking hubs that form a link between membrane fusion, organelle motility and signaling. CORVET, CHEVI and HOPS are MTCs of the endo-lysosomal system. They regulate the major membrane flows required for endocytosis, lysosome biogenesis, autophagy and phagocytosis. In addition, individual subunits control complex-independent transport of specific cargoes and exert functions beyond tethering, such as attachment to microtubules and SNARE activation. Mutations in CHEVI subunits lead to arthrogryposis, renal dysfunction and cholestasis (ARC) syndrome, while defects in CORVET and, particularly, HOPS are associated with neurodegeneration, pigmentation disorders, liver malfunction and various forms of cancer. Diseases and phenotypes, however, vary per affected subunit and a concise overview of MTC protein function and associated human pathologies is currently lacking. Here, we provide an integrated overview on the cellular functions and pathological defects associated with CORVET, CHEVI or HOPS proteins, both with regard to their complexes and as individual subunits. The combination of these data provides novel insights into how mutations in endo-lysosomal proteins lead to human pathologies.

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Section: Cancermentioning

confidence: 99%

CORVET, CHEVI and HOPS – multisubunit tethers of the endo-lysosomal system in health and disease

Beek

Jonker

Welle

et al. 2019

Journal of Cell Science

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“…Genome-wide association studies on lung cancer, lung function, and COPD have identified a number of overlapping Bsusceptibility^loci. With stringent phenotyping, several overlapping loci are independently associated with both COPD and lung cancer, but with pulmonary inflammation and apoptotic processes mediated by the bronchial epithelium (Bondarczuk and PiotrowskaSeget 2013;Corbel et al 2002;Bao et al 2016a). Some lung cancer-specific genetic variants were identified as BCOPD-related^genetic variants associated with clinical variables (Young et al 2011).…”

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confidence: 99%

New biomarkers and therapeutics can be discovered during COPD-lung cancer transition

Wang

2016

Cell Biol Toxicol

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Chronic obstructive pulmonary disease (COPD) has been found to be associated with lung cancer regardless of a patient's smoking history. Of 11,888 incident cases of lung cancer, 23 % had a prior diagnosis of COPD compared with only 6 % of the 37,605 controls (Powell et al. 2013). The prevalence of COPD in lung cancer patients varies from 8 to 50 %, and the annual incidence of lung cancer arising from COPD is 0.8-1.2 %. This indicates that ∼1 % of COPD patients develop lung cancer each year, while only 0.2 % of patients with normal pulmonary function develop lung cancer. The Environment and Genetics in a Lung Cancer Etiology population-based case-control study showed that lung cancer risk was increased among individuals with chronic bronchitis, emphysema, and COPD (Sekine et al. 2012). COPD co-exists with 40-70 % of lung cancer patients, and 50 % of newly diagnosed lung cancer patients had COPD whereas only 8 % of smokers without lung cancer had COPD. Smokers with COPD are more susceptible to lung cancer.Epidemiological studies indicate that tobacco smoke exposure accounts for nearly 90 % of cases of COPD and lung cancer. However, genetic factors may explain why 10-30 % of smokers develop to COPD, even though genetic network and gene set enrichment in cigarette smoking were found to be correlated with the development of lung cancer (Fang et al. 2013). COPD is closely linked to susceptibility to lung cancer and acts as the most important risk factor for lung cancer among smokers, predating lung cancer in up to 80 % of cases. Genome-wide association studies on lung cancer, lung function, and COPD have identified a number of overlapping Bsusceptibility^loci. With stringent phenotyping, several overlapping loci are independently associated with both COPD and lung cancer, but with pulmonary inflammation and apoptotic processes mediated by the bronchial epithelium (Bondarczuk and PiotrowskaSeget 2013;Corbel et al. 2002;Bao et al. 2016a). Some lung cancer-specific genetic variants were identified as BCOPD-related^genetic variants associated with clinical variables (Young et al. 2011).Gene and protein expression profiles were initially investigated among patients with stable COPD, acute exacerbation of COPD (AECOPD), COPD with or without smoking, and COPD with or without lung cancer, to compare with those of healthy or health smokers (Chen et al. 2012). A number of disease-, stage-, duration-, or therapy-specific biomarkers were selected to screen susceptible populations of COPD or lung cancer. Using clinical bioinformatic techniques, the specificity, biological function, or prevalence of selected target genes or proteins from patients with AECOPD were furthermore validated in association with different types, survival rate, or potential mechanism of lung cancer (Ye et al. 2015). Chronic inflammation associated with COPD likely plays a role in the pathogenesis of lung cancer, and acute exacerbation can be the critical factor in the tumorigenesis of lung cancer. Inflammation

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“…For example, the expression of CCL20 in lung cancer cells is higher in patients with advanced lung cancer than in patients with early-stage lung cancer, and this high expression is associated with a poor prognosis. Bao et al reported that the CCL20 gene may be a prognostic risk factor or protective factor for lung adenocarcinoma [28]. These observations mean that the unstable expression of these genes can cause different oncological outcomes.…”

Section: Discussionmentioning

confidence: 99%

IRGS: an immune-related gene classifier for lung adenocarcinoma prognosis

Shi

Dong

et al. 2020

J Transl Med

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Background: Tumour cells interfere with normal immune functions by affecting the expression of some immunerelated genes, which play roles in the prognosis of cancer patients. In recent years, immunotherapy for tumours has been widely studied, but a practical prognostic model based on immune-related genes in lung adenocarcinoma comparable to existing model has not been established and reported. Methods: We first obtained publicly accessible lung adenocarcinoma RNA expression data from The Cancer Genome Atlas (TCGA) for differential gene expression analysis and then filtered immune-related genes based on the ImmPort database. By using the lasso algorithm and multivariate Cox Proportional-Hazards (CoxPH) regression analysis, we identified candidate genes for model development and validation. The robustness of the model was further examined by comparing the model with three established gene models. Results: Gene expression data from a total of 524 lung adenocarcinoma patients from TCGA were used for model development. We identified four biomarkers (MAP3K8, CCL20, VEGFC, and ANGPTL4) that could predict overall survival in lung adenocarcinoma (HR = 1.98, 95% CI 1.48 to 2.64, P = 4.19e−06) and this model could be used as a classifier for the evaluation of low-risk and high-risk groups. This model was validated with independent microarray data and was highly comparable with previously reported gene expression signatures for lung adenocarcinoma prognosis. Conclusions: In this study, we identified a practical and robust four-gene prognostic model based on an immune gene dataset with cross-platform compatibility. This model has potential value in improving TNM staging for survival predictions in patients with lung adenocarcinoma. Impact: The study provides a method of immune relevant gene prognosis model and the identification of immune gene classifier for the prediction of lung adenocarcinoma prognosis with RNA sequencing and microarray compatibility.

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Variations of chromosome 2 gene expressions among patients with lung cancer or non-cancer

Cited by 50 publications

References 47 publications

CORVET, CHEVI and HOPS – multisubunit tethers of the endo-lysosomal system in health and disease

CORVET, CHEVI and HOPS – multisubunit tethers of the endo-lysosomal system in health and disease

New biomarkers and therapeutics can be discovered during COPD-lung cancer transition

IRGS: an immune-related gene classifier for lung adenocarcinoma prognosis

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