Epigenetic changes of stromal-epithelial interactions are of key importance in the regulation of colorectal carcinoma (CRC) cells and morphologically normal, but genetically and epigenetically altered epithelium in normal adjacent tumor (NAT) areas. Here we demonstrated retained protein expression of well-known Wnt inhibitor, secreted frizzled-related protein 1 (SFRP1) in stromal myofibroblasts and decreasing epithelial expression from NAT tissues towards the tumor. SFRP1 was unmethylated in laser microdissected myofibroblasts and partially hypermethylated in epithelial cells in these areas. In contrast, we found epigenetically silenced myofibroblast-derived SFRP1 in CRC stroma. Our results suggest that the myofibroblast-derived SFRP1 protein might be a paracrine inhibitor of epithelial proliferation in NAT areas and loss of this signal may support tumor proliferation in CRC.

/pdf/myofibroblast-derived-sfrp1-as-potential-inhibitor-of-125n5e82fu.pdf

Myofibroblast-derived SFRP1 as potential inhibitor of colorectal carcinoma field effect.

Pulmonary fibrosis, lung cancer and chronic obstructive pulmonary disease (COPD) are severe diseases and common death causes worldwide. Due to the lack of an effective therapy, the investigation of cell biological mechanisms behind these diseases is essential. An activation of stromal cells, including myofibroblasts, is a main feature found in the pathogenesis of lung diseases. Myofibroblasts express alpha-smooth muscle actin (α-SMA), have specific ultrastructure, produce extracellular matrix proteins and possess contractile capacity. Detailed structure and function of myofibroblasts and their roles in healthy and diseased lung are not yet wholly understood. The investigation of the myofibroblasts may further offer novel tools for the acquisition of proper diagnosis, prognosis and medical treatment. The study aimed to characterize the ultrastructural, functional and disease-specific features of stromal cells, particularly myofibroblasts, in interstitial and malignant lung diseases. The functional properties evaluated here were differentiation, invasive and contractile properties. The study material included in vitro stromal cells cultured from bronchoalveolar lavage (BAL) fluids. The appearance and location of myofibroblasts in different lung compartments of non-smokers and the COPD-patients were examined in vivo. The cells were investigated by light and electron microscopy. The α-SMA expression was analysed by gene or protein assays. The study demonstrated that stromal cells could be cultured from diagnostic BAL fluid samples and lung tissues. Cultured cells were a mixture of fibroblasts and myofibroblasts. A small proportion of cells exhibited progenitor-like features. Myofibroblasts revealed differential features in electron microscopy and invasive or contractile assays. When studying tissues from healthy and COPD lungs, myofibroblasts were located both in alveoli and airways. In alveoli myofibroblasts localized in widened alveolar tips which were newly described structures and locations of myofibroblasts in healthy and diseased lung. The amount of myofibroblasts in large airways, but not in peripheral lung, was increased in COPD. We concluded that myofibroblasts have several locations in normal and COPD lung, which suggests a function both in pulmonary regeneration and the pathogenesis of COPD. Smoking altered the phenotype of myofibroblasts regardless of its origin.

/pdf/ultrastructural-and-functional-characterization-of-5f1cdyo9v6.pdf

Ultrastructural and functional characterization of myofibroblasts in lung diseases

Modeling the epithelial-mesenchymal transition process in a 3D organotypic cervical neoplasia.

Cystic fibrosis is characterized by lung dysfunction involving mucus hypersecretion, bacterial infections, and inflammatory response. Inflammation triggers pro-fibrotic signals that compromise lung structure and function. At present, several in vitro cystic fibrosis models have been developed to study epithelial dysfunction but none of these focuses on stromal alterations. Here we show a new cystic fibrosis 3D stromal lung model made up of primary fibroblasts embedded in their own extracellular matrix and investigate its morphological and transcriptomic features. Cystic fibrosis fibroblasts showed a high proliferation rate and produced an abundant and chaotic matrix with increased protein content and elastic modulus. More interesting, they had enhanced pro-fibrotic markers and genes involved in epithelial function and inflammatory response. In conclusion, our study reveals that cystic fibrosis fibroblasts maintain in vitro an activated pro-fibrotic state. This abnormality may play in vivo a role in the modulation of epithelial and inflammatory cell behavior and lung remodeling. We argue that the proposed bioengineered model may provide new insights on epithelial/stromal/inflammatory cells crosstalk in cystic fibrosis, paving the way for novel therapeutic strategies.

Intrinsic Abnormalities of Cystic Fibrosis Airway Connective Tissue Revealed by an In Vitro 3D Stromal Model

Aims: To evaluate the potential role of interleukin-31 and interleukin-33 in diagnosis and prognosis from endometrial cancer. Methods: Tissue samples and clinical data were collected from 260 patients with endometrial cancer and 150 control patients with benign uterine diseases. Immunohistochemistry and ELISA testing quantified the expressions of interleukin-31 and interleukin-33 and their receptors. After surgery, all patients were followed up for an average of 56.3 months. Surgical effects were evaluated based on the patients' symptoms and signs. A two-sided P value <0.05 was considered significant. Results: IL-31, IL-33 and their receptors were significantly accumulated with the progression of endometrial cancer, in comparison to the controls. Moreover, the expressions were correlated with clinical characteristics, including tumor stage, differentiation, and associated with patients' disease-free survival. Conclusions: Limited data was available between the expressions of IL-31 and IL-33 and the receptors in patients with endometrial cancer. Our study findings suggested that the expressions of IL-31 and IL-33 might become possible biomarkers for the diagnosis and prediction in endometrial cancer.

Potential clinical value of interleukin-31 and interleukin-33 with their receptors expression as diagnostic and predictive factors in endometrial cancer: a case-control study.

Identification of gene expression mechanisms began with works on embryonic induction. The same mechanism of cell-cell interactions also contributes to the process of oncogenesis. Damage to epithelial cells’ genetic apparatus turns them into precancerous stem cells that are not yet capable of tumor growth. They can be transformed into cancer stem cells and undergo further progression as a result of epigenetic effects of apocrine secretion by surrounding activated stromal cells (mostly myofibroblasts). These factors may activate the damaged genetic information. On the contrary, the level of malignancy can be decreased by adding culture medium from non-activated stromal cells. One must not exclude the possibility that in a number of cases genetically altered bone marrow may migrate to damaged or inflamed tissues and become there a source of stromal cells, as well as of parenchymal stem cells in a damaged organ, where they may give rise to changed epithelial (precancerous) stem cells or to activated stromal cells, thus leading to malignant tumor growth. Cancer treatment should also affect activated stromal cells. It may prevent emergence and progression of cancerous stem cells.

Role of Stromal-Epithelial Interaction in the Formation and Development of Cancer Cells

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Role of Stromal-Epithelial Interaction in the Formation and Development of Cancer Cells