Markers of Stroma in Lung Cancer: Influence of COPD

Tang, Jun; Ramis-Cabrer, Daniel; Curull, Víctor; Mateu-Jiménez, Mercè; Almagro, Klara; Durán, Xavier; Pijuán, Lara; Rodríguez-Fuster, Alberto; Aguiló, Rafael; Barreiro, Esther

doi:10.1016/j.arbr.2020.09.005

Cited by 1 publication

(2 citation statements)

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“…Several growth factors initiate and maintain EMT within tissues, particularly transforming growth factor (TGF)-β [ 20 , 21 ]. TGF-β has been consistently shown to increase in the systemic compartment and lungs of patients with LC, particularly in those with COPD [ 9 , 22 ]. In a previous investigation [ 23 ], we clearly demonstrated that TGF-β expression levels were significantly greater in lung tumours compared to non-tumour control tissues, and in patients with COPD those levels were, indeed, significantly higher than in tumour specimens of non-COPD patients.…”

Section: Discussionmentioning

confidence: 99%

“…Several biological mechanisms have been shown to participate in the greater risk for LC development in COPD patients [ 5 ]. For instance, increased oxidative stress [ 6 ], inflammation including a differential inflammatory profile [ 7 ], epigenetics abnormalities [ 8 ] and the pattern of expression of stroma markers [ 9 ] have all been demonstrated to be differentially expressed in tumours of patients with mild-to-moderate COPD. In addition, overall survival was also shown to be significantly altered on the basis of the inflammatory profile in lung tumours of patients with underlying COPD compared to LC patients without COPD [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Gene expression profile of epithelial–mesenchymal transition in tumours of patients with nonsmall cell lung cancer: the influence of COPD

et al. 2022

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Epithelial-mesenchymal transition (EMT) is involved in the pathophysiology of lung cancer (LC) and chronic obstructive pulmonary disease (COPD), and the latter is an important risk factor for LC. We hypothesized that gene expression profile of EMT and signaling cascade may differ in LC patients with COPD from those with no respiratory diseases. In lung tumor specimens obtained through video-assisted thoracoscopic surgery (VATS) from LC (n=20, control group) and LC-COPD patients (n=30), gene expression (qRT-PCR) of EMT markers: SMAD3, SMAD4, ZEB2, TWIST1, SNAI1, ICAM1, VIM, CDH2, MMP1, and MMP9 were detected. In lung tumors of LC-COPD compared to LC patients, gene expression of SMAD3, SMAD4, ZEB2, and CDH2 significantly declined, while no significant differences were detected for the other analyzed markers. A significant correlation was found between packs-years (smoking burden) and SMAD3 gene expression among LC-COPD patients. LC-COPD patients exhibited mild-to-moderate airway obstruction and a significant reduction in diffusion capacity compared to LC patients. In lung tumor samples of patients with COPD, several markers of EMT expression, namely SMAD3, SMAD4, ZEB2, and CDH2 were differentially expressed suggesting that these markers are likely to play a role in the regulation of EMT in patients with this respiratory disease. Cigarette smoke did not seem to influence the expression of EMT markers in this study. These results have potential clinical implications in the management of patients with LC, particularly in those with underlying respiratory diseases.

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