Markers of Stroma in Lung Cancer: Influence of COPD

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

doi:10.1016/j.arbres.2020.09.005

Cited by 5 publications

(3 citation statements)

References 28 publications

(4 reference statements)

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“…Underlying respiratory conditions favor the incidence of lung tumors in patients, especially in those with emphysema [8,9]. Mechanisms such as inflammation, oxidative stress, epigenetics alterations, and the tumor microenvironment underlie the pathophysiology of tumor development in patients with chronic respiratory disorders including stromal structures and immune cell profiles, and have an impact on the patients' survival [10][11][12]. Indeed, chronic obstructive pulmonary disease (COPD) is a major risk factor for LC development [9,13].…”

Section: Introductionmentioning

confidence: 99%

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Tang

Curull

Wang

et al. 2020

Cancers

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(1) Background: Lung cancer (LC) is a major leading cause of death worldwide. Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 are key players in cancer. We aimed to assess PARP-1 and PARP-2 expression and activity and DNA damage in tumors and non-tumor lungs from patients with/without chronic obstructive pulmonary disease (COPD). (2) Methods: Lung tumor and non-tumor specimens were obtained through video-assisted thoracoscopic surgery (VATS) in LC patients with/without underlying COPD (two groups of patients, n = 15/group). PARP-1 and PARP-2 expression (ELISA), PARP activity (PARP colorimetric assay kit) and DNA damage (immunohistochemistry) levels were identified in all samples. (3) Results: Both PARP-1 and PARP-2 expression levels were significantly lower in lung tumors (irrespective of COPD)compared to non-tumor specimens, while DNA damage and PARP activity levels significantly increased in lung tumors compared to non-tumor specimens only in LC-COPD patients. PARP-2 expression was positively correlated with smoking burden in LC-COPD patients. (4) Conclusions: In lung tumors of COPD patients, an overactivation of PARP enzyme was observed. A decline in PARP-1 and PARP-2 protein expression was seen in lung tumors irrespective of COPD. Other phenotypic features (airway obstruction) beyond cancer may account for the increase in PARP activity seen in the tumors of patients with underlying COPD.

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Section: Introductionmentioning

confidence: 99%

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Tang

Curull

Wang

et al. 2020

Cancers

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“…In patients with COPD, particularly in emphysema phenotype, LC development was five times greater than in smokers with no COPD [4,5]. Recently, our group and others have demonstrated the implications of relevant biological mechanisms in the increased LC predisposition seen in patients with COPD [6][7][8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 86%

Systemic Profiles of microRNAs, Redox Balance, and Inflammation in Lung Cancer Patients: Influence of COPD

et al. 2021

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Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients.

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“…Cancer-associated fibroblasts (CAFs), the most common type of stromal cells, are an important source of extracellular matrix (ECM)-degrading proteases, such as matrix metalloproteinases (MMPs), which play several important roles in tumorigenesis. Depending on the substrate, MMPs can promote invasion, angiogenesis, recruitment of inflammatory cells, and metastasis through ECM degradation [8].…”

Section: Introductionmentioning

confidence: 99%

Metastatic prognostic ability of lung cancer stromal cells from a single-cell RNA-seq perspective

Moon

Kim

Jeon

et al. 2023

Preprint

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Single-cell RNA sequencing (scRNA-seq) has been widely studied and analyzed to understand cancer heterogeneity. Metastasis and invasion through communication with immune cells have been widely studied; stromal cells are known to change during cancer progression and cause metastasis, but little is known about their inherent metastasis prognostic abilities. This study investigated the abilities of stromal cells by analyzing the scRNA-seq data of adjacent, tumor, and metastasized tissues, biopsied from 15 patients. We considered fibroblast and smooth muscle cells as cell subtypes of stromal cells. We detected decorin (DCN) and insulin-like growth factor-binding protein 7 (IGFBP7) as sub-cell type markers conserved in tumor and metastasis. We found an organic relationship that affects metastasis by assessing the interaction between the expression and related pathways among the assigned stromal cell subtypes. In addition to the interactions of sub-cell-types within stromal cells, we also studied communication between stromal cells and the five assigned lung cancer cell types, and observed its relation with migration and metastasis; the role of DCN as a mediating factor was also studied. Results of our study indicated that DCN and IGFBP7 are factors that can be monitored in the follow-up of prognostic metastasis factors in patients with lung cancer. Therefore, DCN and IGFBP7, which are the assigned sub-cell types marker in lung cancer stromal cells, can be used as potential biomarkers for follow-up in lung cancer metastasis. Our study assigned stromal cell subtypes of lung cancer and detected markers that can be used as monitoring factors during metastasis of lung cancer. This suggests that DCN and IGFBP7 are potential biomarkers to evaluate metastatic ability and follow-up as metastatic prognostic factors in lung cancer patients.

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Markers of Stroma in Lung Cancer: Influence of COPD

Cited by 5 publications

References 28 publications

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Systemic Profiles of microRNAs, Redox Balance, and Inflammation in Lung Cancer Patients: Influence of COPD

Metastatic prognostic ability of lung cancer stromal cells from a single-cell RNA-seq perspective

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