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© Borgis - Postępy Nauk Medycznych 4/2020, s. 105-110 | DOI: 10.25121/PNM.2020.33.4.105
Pawel Zarebski1, *Anna Zubkiewicz2, Agnieszka Zubkiewicz-Kucharska3
Do adhesive molecules ICAM-1 and VCAM-1 affect the development and course of gastrointestinal tumors?
Czy molekuły adhezyjne ICAM-1 i VCAM-1 wpływają na rozwój i przebieg nowotworów przewodu pokarmowego?
12nd Department and Clinic of General and Oncological Surgery, Wroclaw Medical University, Poland
2Department and Clinic of Gastroenterology and Hepatology, Wroclaw Medical University, Poland
3Department and Clinic of Endocrinology and Diabetology for Children and Adolescents, Wroclaw Medical University, Poland
Streszczenie
Guzy lite zbudowane są z dwóch części: komórek zmienionych nowotworowo, stanowiących zasadniczą masę guza, i komórek podścieliska nowotworu. Interakcje komórka-komórka i komórka-macierz zewnątrzkomórkowa zachodzą przy udziale molekuł adhezyjnych (CAM) i wpływają na wzrost, różnicowanie i migrację komórek guza. Nieprawidłowa ekspresja CAM leży u podstaw zaburzeń morfologicznych, utraty połączeń międzykomórkowych, dezorganizacji cytoszkieletu, co pozwala komórkom nowotworowym na oderwanie się od masy guza i przerzutowanie.
Celem tej pracy jest przedstawienie aktualnego stanu wiedzy i wyników nowych badań dotyczących ekspresji wybranych molekuł adhezyjnych: ICAM-1 i VCAM-1 u chorych na raka przełyku, żołądka i jelita grubego.
W ostatnim czasie obserwuje się nasilenie badań molekuł adhezyjnych w licznych nowotworach. Dowiedziono, że ICAM-1 uczestniczy we wszystkich etapach ontogenezy, od bardzo wczesnych stadiów zapalnych poprzez etap adhezji komórek guza i leukocytów do komórek endotelium, do późnego etapu migracji komórek nowotworowych i zasiedlania kolejnych narządów. Interakcja ICAM-1 gospodarza z ligandem na komórce guza i komórce gospodarza w czasie kolejnych etapów przerzutowania może stać się atrakcyjnym celem leczenia przeciwnowotworowego. Badania wykazały, że VCAM-1 odgrywa istotną rolę w procesie adhezji komórek guza do komórek endotelium oraz w procesie neowaskularyzacji.
Stężenie rozpuszczalnego VCAM-1 w surowicy koreluje z ekspresją VCAM-1 w tkance guza i ulega istotnemu zmniejszeniu po operacyjnym usunięciu nowotworu. W tym aspekcie sVCAM-1 może być traktowany jako czuły marker diagnostyczny i prognostyczny.
Summary
Solid tumors are composed of two compartments: cancerous cells constituting the essential mass of tumor and stromal tumor cells. Cell-cell and extracellular matrix-cell interactions are mediated by adhesive molecules (CAMs, cell adhesion molecules) and affect the growth, differentiation and migration of tumor cells. Abnormal ICAM expression may underlie in morphological disturbances, loss of cell-to-cell junctions, cytoskeleton disorganization, allowing cancer cells to detach from tumor mass and metastase.
The aim of this work is to present the current state of knowledge and results of new research on the expression of selected adhesion molecules: ICAM-1 and VCAM-1 in patients with esophageal, gastric and colorectal cancer.
Recently, the research of adhesion molecules in numerous cancers has been observed. It has been demonstrated that ICAM-1 participates in all stages of oncogenesis. The interaction of the host ICAM-1 with a ligand on a tumor cell and host cell during subsequent metastatic stages may become an attractive target for anticancer treatment. Studies have shown that VCAM-1 plays an important role in the process of tumor cell adhesion to endothelial cells and in the neovascularization process.
The concentration of soluble VCAM-1 in serum correlates with the expression of VCAM-1 in tumor tissue, and is significantly reduced after surgical removal of the tumor. In this aspect sVCAM-1 can be treated as a sensitive diagnostic and prognostic marker.



Introduction
Solid tumors are composed of two compartments: cancerous cells constituting the essential mass of tumor and stromal tumor cells. Tumor cells induce the formation of stroma, which is formed of connective tissue and blood vessels, and protects nutrition and gas exchange of tumor cells. Cell-cell and extracellular matrix-cell interactions are mediated by adhesive molecules (CAMs, cell adhesion molecules) and affect the growth, differentiation and migration of tumor cells (1). Abnormal ICAM expression may underlie in morphological disturbances, loss of cell-to-cell junctions, cytoskeleton disorganization, allowing cancer cells to detach from tumor mass and metastase. The adhesins allow tumor cells to stimulate angiogenesis and affect the formation of a metastase (2). The formation of new vessels is necessary to increase the tumor mass of both primary and metastatic lesions (3). The pre-cancerous state or the site of the secondary tumor focus may be inflammation, which is determined by the chemotactic action of pro-inflammatory cytokines as well as by the presence of adhesion molecules on the activated endothelium (2). Thus, tumor progression and its expansion into distant organs is strongly dependent on adhesion molecules, Numerous studies have shown that the clinical stage of the disease is a key prognostic parameter for the survival and recurrence of cancer (4). This means that the features characteristics for cancer cells such as the ability to survive, growth and forming metastatic leasions affect the overall survival of cancer patients, including esophageal, gastric and colorectal cancers.
The studies carried out in the last quarter of a century prove that adhesion molecules, on the one hand, participate in various stages of tumor angiogenesis, participate in its progression and metastasis, but on the other hand, adhesins, suppressor gene expression products have anticancer properties.
The aim of this work is to present the current state of knowledge and results of new research on the expression of selected adhesion molecules: ICAM-1 and VCAM-1 in patients with esophageal, gastric and colorectal cancer.
ICAM-1, VCAM-1: Adhesion molecules from the immunoglobulin superfamily
Intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) belong to adhesion molecules from the immunoglobulin superfamily (IgCAM, immunoglobin cell adhesion molecule, IgSf, Immunoglobin Superfamily), to IgCAM system group (5).
ICAM-1 is glycoprotein with 80-114 kDa mass, the gene coding this protein is located on the short arm of chromosome 19 (19p13.2) (6). ICAM-1 occurs on the surface of endothelial cells, epithelial cells, e.g. thymus, fibroblasts, smooth muscle cells, and hematopoietic cells, e.g. on tissue macrophages, lymphoblasts, tonsil dendritic cells, lymph nodes and Peyer’s patches. ICAM-1 plays an important role during a specific and unspecific immune response. ICAM-1 as major ligand for LFA-1 (lymphocyte function antigen 1) is an important factor in the process immunosurveillance (7). Strong ICAM-1 expression on lymphoma cells was demonstrated during transplant rejection and atherosclerotic lesions (8-10). ICAM-1 is a receptor for erythrocytes infected with Plasmodium falciparum, rhinoviruses, as well as some neurotrophic viruses, e.g. West Nile virus, Semliki Forest virus (SMV) and others (11, 12).
In the last decade, the relationship between the inflammatory process, insulin resistance, and disorders of carbohydrate metabolism and hypertension has been proven. The Salmenniemi study conducted on the obese adult group confirmed the relationship between ICAM-1 concentration and the occurrence of metabolic syndrome (13).
The vascular cell adhesion molecule 1 (VCAM-1) is a transmembrane glycoprotein of 110 kDa mass, made of 739 amino acids. The VCAM-1 coding gene is located on the short arm of chromosome 1 (1p21.2) (14). VCAM-1 expression induces proinflammatory reaction: IL-1, TNF-α or IFN-γ and lipopolysaccharides (LPS), mechanical factors – disturbed blood flow, and reactive oxygen species (ROS), lower antioxidants, ω-3 acids and nitric oxide. In 1990, VLA-4 (very late activation antigen-4) was identified, the first VCAM-1 ligand mediating B-cell adhesions in germinal centers (15). VCAM-1 was shown to be involved in the pathogenesis of autoimmune diseases, cardiovascular disease and infections (16). The main task of VCAM-1 is to control the movement of leukocytes, (with the exception of neutrofils on which VLA-4 is absent) across the endothelial barrier. Under the influence of proinflammatory cytokines, endothelial cells increase the expression of VCAM-1, which promotes adherence of monocytes to endothelial cells and is necessary in their migration. VCAM-1, which is absent at the resting endothelium cells, is detectable on dendritic cells of the lymph nodes, macrophages, bone marrow fibroblasts as well as on tumor cells, e.g. in acute lymphoblastic leukemia and acute myeloblastic leukemia, and in some central nervous system tumors (17).
ICAM-1 as a marker of neoplastic and autoimmune diseases
The involvement of adhesins in the pathogenesis of cancer and metastasis was the basis for their use in diagnostics and prognosis of cancers of lung, breast, genitourinary system, melanoma, pancreas and gastrointestinal tract. The combination of ICAM-1 on a tumor cell with LFA-1 on the surface of T lymphocytes results in an increase in their cytotoxic activity and sensitivity of tumor cells to lymphocyte-dependent cytotoxicity (18). It has been demonstrated that prostaglandin E2, produced by tumor stromal cells, inhibits the expression of ICAM-1 and thus reduces the cytotoxic effect of T lymphocytes (19). Such ICAM-1 activity could justify the results of research in breast, gastric and colorectal cancers, according to which an increase in ICAM-1 expression on cancer cells correlated with a better prognosis (20).
On the other hand, Schröder’s and Rosette’s observations showed a positive correlation between the expression of ICAM-1 and a more aggressive phenotype and greater metastatic potential in breast cancer (21, 22). Usami study in oral squamous cell carcinoma (SCC) have shown that ICAM-1 was expressed predominantly at the invasive front area of tongue SCC and correlated with invasion, lymph node metastasis and increased blood and lymphatic vessel density of the tongue SCC. Increased ICAM-1 expression in tongue SCC was correlated with increased macrophage infiltration within SCC nests. These findings indicate that ICAM-1 plays an important role in tongue SCC progression, which may result from the SCC-cell activity, angiogenic activity, lymphangiogenic activity and macrophage/SCC-cell adhesion (23).

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otrzymano: 2020-10-07
zaakceptowano do druku: 2020-10-28

Adres do korespondencji:
*Anna Zubkiewicz
Department and Clinic of Gastroenterology and Hepatology Wroclaw Medical University
ul. Borowska 213, 50-556 Wroclaw, Poland
tel.: +48 (71) 733-21-20
a.w.zubkiewicz@gmail.com

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