Extracellular sulfatases as potential blood-based biomarkers for early detection of lung cancer

Yang, Yiwei; Jablons, David M.; Lemjabbar-Alaoui, Hassan

doi:10.1080/01902148.2021.1885525

Cited by 2 publications

(2 citation statements)

References 21 publications

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“…41 SULF1 gene expression was found to be elevated in various cancers. 42,43 These results are inconsistent with the results of previous studies, which considered SULF1 to be a tumor suppressor. 44 This effect may be related to the alternative splicing of the Sulf1 gene.…”

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confidence: 89%

“… 45 SULF2 levels in the serum of COPD patients has been found to be elevated, but there have not been any recent studies conducted on SULF1 in COPD. 43 At present, SULF1 has been confirmed to be significantly elevated in a mouse emphysema model and in vitro in bronchial epithelial cells stimulated by tobacco smoke, but its specific mechanism of action on the pathogenesis of COPD needs to be further elucidated. POU2AF1, previously thought to be expressed specifically in lymphocytes, regulates the expression of immunoglobulin and other host defense genes.…”

Section: Discussionmentioning

confidence: 92%

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Identification of Hub Genes Associated with COPD Through Integrated Bioinformatics Analysis

Chen¹,

Zhu²,

Huang³

et al. 2022

COPD

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Smoking is recognized as a risk factor for Chronic Obstructive Pulmonary Disease (COPD), yet only 20-25% of smokers eventually develop COPD. Since its molecular pathogenesis remains unclear, there is an important need to further understand genetic differences between smokers with COPD and healthy smokers, screen out high-risk and susceptible groups among smokers, and find effective therapeutic targets. Methods: Bioinformatics tools were used to screen biomarkers that were significantly associated with COPD smokers and healthy smokers. qRT-PCR and Western blotting analysis were used to detect hub gene expression in CSE-treated BEAS-2B cells and lung tissue of COPD mouse models. Results: Our study identified 132 DEGs. The GO and KEGG analyses suggested that the ECM-receptor interaction, MAPK signaling pathway, Chemokine signaling pathway, PI3K-Akt signaling pathway, extracellular matrix organization and collagen fibril organization were associated with the occurrence and development of COPD. In addition, WGCNA analysis of GSE1650 showed that the brown module was most correlated with COPD. The intersection between the brown module and DEGs was used to identify 9 HUB genes (COL14A1, SULF1, MOXD1, CXCL12, CHRNA1, COMP, POU2AF1, MMP11, THBS2) that showed consistent expression and upregulation. Both the mRNA and protein expression levels of the Hub genes (except that of MMP11) were significantly upregulated in tobacco smoke exposed mouse emphysema models and CSE treated BEAS-2B cells. Conclusion:Our results suggest that COL14A1, SULF1, MOXD1, CXCL12, CHRNA1, COMP, POU2AF1, and THBS2 may be potentially useful biomarkers for identifying smokers with a risk of developing COPD. The GO and KEGG functional enrichment analyses further confirmed the significant role played by ECM in the pathogenesis of COPD. The results of this study may provide further insights into the pathogenetic mechanisms involved in COPD.

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confidence: 89%

Section: Discussionmentioning

confidence: 92%