Surveying the expression of CDH1 and EGFR
Anthracosis is the pneumoconiosis caused by exposure to coal dust [24]. The term “anthracotic” refers to coal particles and other black pigments of which carbon is the main element [25, 26]. Coal particles, mostly in the coalmine workers and to a less extent in city dweller, are found in the background of vocational and air pollution diseases as sediment at mucosa and submucosa; and under bronchoscopy, they appear as black lesions with normal or deformed bronchus with high fragility [25, 26].
In addition to coalmine workers, the disease is found among workers in the industries related to coal [25]. In fact, occupational exposure to carbon, silicon dioxide, and quartz at work are the known causes of pulmonary anthracosis; although, there are cases without any pertinent occupation history as well [28]. In other words, anthracosis is an outcome of aggregation of carbon in the lungs after long and frequent exposure to air pollution and inhaling smock and coal dust [29]. In addition to the lungs, there are reports of anthracosis in the liver, spleen, and esophagus; the latter case should be considered as a serious disease as it demonstrates malignant melanoma [65, 66]. In some cases, an anthracosis case is misdiagnosed as tuberculosis, lung carcinoma, or pneumonia [71].
Cytology studies on pulmonary tissues have shown that inter-bronchus anthracosis and lymphadenopathy mediastinum are concurrent with the early endocardium. Thereby, there is a probably significant relationship between anthracosis and lung carcinoma [75].
Lung carcinoma is the most common type of cancer in men and more than 80% of the patients die during the first five years after diagnosis [30, 30].
CDH1 gene encodes E-Cadherin protein [133] and it is a tumor suppressor gene with a key role in preserving cellular adhesion and stable connections in normal tissues through expression of Cadherin1 protein. In addition, the gene keeps epithelium cells in their normal layer and arrangement [138].
The role of E-Cadherin in signaling indicates that the molecule can demonstrate different functions so that it can regulate the cell response to the external signals received by the cell. Therefore, it can regulate migration, proliferation, apoptosis, and cell differentiation [139].
Failure of CDH1 function facilitates progress of cancer via the increase of proliferation, invasion, and metastasis [138]. The decrease of E-cadherin expression is a main molecular event effective on the failure of inter-cell adhesion system, cancer invasion, and metastasis [139].
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