Abstract
BackgroundMetastasis occurs in a series of discrete steps involving invasion, angiogenesis, lymphovascular space permeation, and establishment of secondary tumors. Malignant pleural effusion (MPE), a type of tumor metastasis, is usually a poor prognostic sign for patients with pulmonary adenocarcinoma, although its underlying mechanism has received less attention than other types of metastases have. The objective of the current study was to confirm whether cancer stem cells (CSCs) in MPE contribute to the “metastatic cascade” through the epithelial – mesenchymal transition (EMT), anoikis, and adaptation in the microenvironment.MethodsPulmonary tissue and corresponding cell blocks of MPE samples from 20 patients with primary adenocarcinoma were analyzed by immunohistochemical staining with CSC-representative markers (CD133, Nanog, and OCT-4) and EMT-associated markers (E-cadherin and vimentin). Correlations between these variables and clinico-pathological parameters were analyzed. Primary cultures from eight cases of MPE were investigated to characterize the CSC properties, including marker expression, sphere formation, and differentiation.ResultsExpressions of CSC-representative markers for 20 cases of MPE cell blocks were quite diverse and variable ranging from 15% to 90%. Stronger expression of CSC-representative markers and alteration of EMT-associated markers were found at the invasive fronts and in MPEs compared with the expression in primary pulmonary tumor tissues. The expression of OCT-4 in MPEs significantly related to distant metastasis and stage, as well as inversely correlated with patient survival. Primary cultures confirmed the CSC properties in MPE. Five of eight cases of MPE yielded adequate cell clusters, which also showed variable expressions of CSC markers in addition to sphere formation and the ability for differentiation and metastasis.ConclusionThis pilot study offers a better understanding of the metastatic cascade. Establishing a model of MPE will provide further insight into the role of CSCs in metastasis and may explain the high therapeutic failure rates for patients with MPE.
Highlights
Metastasis, the spread of malignant cells from a primary tumor to distant organs, is the main cause of treatment failure and death in cancer patients [1]
Confirmation and identification of adenocarcinoma in the lung and pleural effusions Tissues from primary pulmonary adenocarcinoma and the corresponding Malignant pleural effusion (MPE) cell blocks from 20 patients were selected as study groups
CEA is of value in confirming the presence of an adenocarcinoma and is considered a better alternative for differentiating between invasive malignant and nonmalignant effusions [19]
Summary
Metastasis, the spread of malignant cells from a primary tumor to distant organs, is the main cause of treatment failure and death in cancer patients [1]. It usually comprises a series of discrete steps and requires the transport of malignant cells via blood and/or lymph vessels. Involvement of the serous membrane from the primary pulmonary adenocarcinoma causing initial malignant pleural effusion (MPE) usually indicates a late stage of cancer. Malignant pleural effusion (MPE), a type of tumor metastasis, is usually a poor prognostic sign for patients with pulmonary adenocarcinoma, its underlying mechanism has received less attention than other types of metastases have. The objective of the current study was to confirm whether cancer stem cells (CSCs) in MPE contribute to the ‘‘metastatic cascade’’ through the epithelial – mesenchymal transition (EMT), anoikis, and adaptation in the microenvironment
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