Cigarette Smoke Induced Lung Barrier Dysfunction, EMT, and Tissue Remodeling: A Possible Link between COPD and Lung Cancer

Abstract

Chronic obstructive pulmonary disease (COPD) and lung cancer, closely related to smoking, are major lung diseases affecting millions of individuals worldwide. The generated gas mixture of smoking is proved to contain about 4,500 components such as carbon monoxide, nicotine, oxidants, fine particulate matter, and aldehydes. These components were considered to be the principle factor driving the pathogenesis and progression of pulmonary disease. A large proportion of lung cancer patients showed a history of COPD, which demonstrated that there might be a close relationship between COPD and lung cancer. In the early stages of smoking, lung barrier provoked protective response and DNA repair are likely to suppress these changes to a certain extent. In the presence of long-term smoking exposure, these mechanisms seem to be malfunctioned and lead to disease progression. The infiltration of inflammatory cells to mucosa, submucosa, and glandular tissue caused by inhaled cigarette smoke is responsible for the destruction of matrix, blood supply shortage, and epithelial cell death. Conversely, cancer cells have the capacity to modulate the proliferation of epithelial cells and produce of new vascular networks. Comprehension understanding of mechanisms responsible for both pathologies is necessary for the prevention and treatment of COPD and lung cancer. In this review, we will summarize related articles and give a glance of possible mechanism between cigarette smoking induced COPD and lung cancer.

Circulating tumor cell analysis in locally advanced and metastatic squamous cell carcinoma of the head and neck

“…This study found that smoking is positively associated with CTC detection on univariate analysis. Smoking has many effects on cell‐to‐cell adhesion, including downregulating E‐cadherin, a tumor suppressor that maintains cell‐cell adhesion, and promoting epithelial to mesenchyme transition (EMT) 22‐29 in various cancers including prostate, lung, and oropharyngeal squamous cell carcinoma 26,30‐32 . Moreover, a key step in EMT is loss of E‐cadherin, leading to invasive behavior and metastasis.…”

Impact of the Local Inflammatory Environment on Mucosal Vitamin D Metabolism and Signaling in Chronic Inflammatory Lung Diseases

“…Diseases such as COPD and asthma are characterized by chronic inflammation, a low-grade and prolonged inflammation that may result in destruction and aberrant repair of surrounding tissue by growth factors, proteases and cytokines that are released at the site of inflammation ( 113 – 115 ). Cumulative data suggest that vitamin D exerts anti-inflammatory effects via its actions on both innate and adaptive immune responses.…”

A Review of the Impact of Smoking on Inhaled Insulin: Would You Stop Smoking if Insulin Can Be Inhaled?

“…Cigarette smoke (CS) consists of two phases, namely the vapor phase and the particulate phase [36]. Earlier estimated to be around 3700, the data now suggests that there are about 4500-4700 particles in CS [35][36][37][38]. The majority of these particles damage or modify the lung in several ways, especially the alveolar region, which is also the site of absorption for inhaled insulin.…”

“…CS affects the cells in several ways. CS causes an influx of inflammatory cells, which is responsible for the destruction of the matrix, reduction in blood supply, and loss of epithelial cells [37]. Not only in the lungs, but CS also causes cutaneous vasoconstriction due to the presence of nicotine, which would also reduce the absorption of subcutaneous insulin [36,43,44].…”