Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity

Königshoff, Mélanie

doi:10.1159/000326299

Cited by 58 publications

(40 citation statements)

References 116 publications

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“…It is important to investigate whether the expression of HS6ST2S contributes to the bronchiolar metaplasia process of the distal lung in IPF. In addition, bronchiolar metaplasia is thought to be a preneoplastic lesion, and IPF is frequently associated with the development of lung cancer (49). On this note, HS6ST2S has been shown to be overexpressed in pancreatic cancer, and silencing of HS6ST2S leads to inhibition of cell invasion and migration and to reduced tumorigenesis (50).…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Heparan Sulfate 6-O-Sulfation in Idiopathic Pulmonary Fibrosis

Auduong

White

et al. 2014

Am J Respir Cell Mol Biol

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Heparan sulfate proteoglycans (HSPGs) are integral components of the lung. Changes in HSPGs have been documented in idiopathic pulmonary fibrosis (IPF). Many of the biological functions of HSPGs are mediated by heparan sulfate (HS) side chains, and little is understood about these side chains in the pathogenesis of IPF. The aims of this study were to compare HS structure between normal and IPF lungs and to examine how changes in HS regulate the fibrotic process. HS disaccharide analysis revealed that HS 6-O-sulfation was significantly increased in IPF lungs compared with normal lungs, concomitant with overexpression of HS 6-O-sulfotransferases 1 and 2 (HS6ST1/2) mRNA. Immunohistochemistry revealed that HS6ST2 was specifically expressed in bronchial epithelial cells, including those lining the honeycomb cysts in IPF lungs, whereas HS6ST1 had a broad expression pattern. Lung fibroblasts in the fibroblastic foci of IPF lungs expressed HS6ST1, and overexpression of HS6ST1 mRNA was observed in primary lung fibroblasts isolated from IPF lungs compared with those from normal lungs. In vitro, small interference RNA-mediated silencing of HS6ST1 in primary normal lung fibroblasts resulted in reduced Smad2 expression and activation and in reduced expression of collagen I and a-smooth muscle actin after TGF-b1 stimulation. Similar results were obtained in primary IPF lung fibroblasts. Furthermore, silencing of HS6ST1 in normal and IPF lung fibroblasts resulted in significant down-regulation of TbRIII (betaglycan). In summary, HS 6-O-sulfation is up-regulated in IPF with overexpression of HS6ST1 and HS6ST2, and overexpression of HS6ST1 in lung fibroblasts may regulate their fibrotic responses to TGF-b1.

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Section: Discussionmentioning

confidence: 99%

Up-Regulation of Heparan Sulfate 6-O-Sulfation in Idiopathic Pulmonary Fibrosis

Auduong

White

et al. 2014

Am J Respir Cell Mol Biol

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“…Secondly, Rexo2 is an RNA exonuclease and recently another similar enzyme, Xrn2 has been associated with murine lung cancer [19] through its involvement in epithelial cell proliferation. Impaired restoration of the alveolar epithelium following the initial stimulus is a potential trigger for pulmonary fibrosis [40,41], therefore variation in a gene implicated in alveolar cell proliferation could contribute to radiation-induced lung damage.…”

Section: Discussionmentioning

confidence: 99%

Genomic and genome-wide association of susceptibility to radiation-induced fibrotic lung disease in mice

Paun¹,

Haston

2012

Radiotherapy and Oncology

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“…Cigarette smoking is the leading cause of lung cancer [6,7] and is related to almost 50–90% of cases [2]. Other risk factors are occupational exposure to carcinogens, passive smoking, air pollution, heavy metals, inorganic dusts, chemical compounds [2,8,9], airflow abstraction, emphysema [10] and pulmonary fibrosis [11]. …”

Section: Introductionmentioning

confidence: 99%

Opium Could Be Considered an Independent Risk Factor for Lung Cancer: A Case-Control Study

Masjedi¹,

Naghan²,

Taslimi

et al. 2012

Respiration

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Background: Lung cancer is the leading cause of cancer-related death worldwide, and half of all incident lung cancers are believed to occur in the developing countries, including Iran. Objective: We investigated the association of opium with the risk of lung cancer in a case-control study. Methods: We enrolled 242 cases and 484 matched controls in this study. A questionnaire was developed, containing questions on basic demographic characteristics, as well as lifelong history of smoking cigarettes, exposure to passive smoking, opium use and alcohol consumption. For smoking cigarettes and opium and also oral opium intake frequency, duration and cumulative use were categorized into three groups: no use, low use and high use. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs). Results: Multivariate analysis in men showed that after adjusting for the effect of ethnicity, education and pack years of smoking cigarettes, smoking opium remained as a significant independent risk factor with an OR of 3.1 (95% CI 1.2–8.1). In addition, concomitant heavy smoking of cigarettes and opium dramatically increased the risk of lung cancer to an OR of 35.0 (95% CI 11.4–107.9). Conclusion: This study demonstrated that smoking opium is associated with a high risk of lung cancer as an independent risk factor.

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Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity

Cited by 58 publications

References 116 publications

Up-Regulation of Heparan Sulfate 6-O-Sulfation in Idiopathic Pulmonary Fibrosis

Up-Regulation of Heparan Sulfate 6-O-Sulfation in Idiopathic Pulmonary Fibrosis

Genomic and genome-wide association of susceptibility to radiation-induced fibrotic lung disease in mice

Opium Could Be Considered an Independent Risk Factor for Lung Cancer: A Case-Control Study

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