Abstract
A search for the “magic bullet”, a molecule, the targeting abilities of which could stop the migration of tumor cells, is currently underway, but remains in the early stages. There are still many unknowns regarding the cell migration. The main approach is the employment of mouse models, that are sources of valuable information, but still cannot answer all of the questions. One of the molecules of interest is Transglutaminase 2 (TG2). It is a well-described molecule involved in numerous pathways and elevated in metastatic tumors. The question remains whether mice and humans can give the same answer considering TG2.
Highlights
Tumors consist of a heterogeneous population of cells, and the heterogeneity is the consequence of genomic instabilities such as chromosomal rearrangements, DNA mutations, and epigenetic changes [1]
The survival of cancer cells that break out into the blood vessels is dependent on their ability to dock and adhere at a distant site, which may explain the increased expression of Transglutaminase 2 (TG2) in metastatic tumors considering its role in cell adhesion [83]
TG2 up-regulation in drug resistant tumors may be connected with its link to a number of survival pathways, since TG2 interaction with integrins and fibronectin on the cell surface may lead to the activation of cell survival and anti-apoptotic signaling pathways [84,85]
Summary
Tumors consist of a heterogeneous population of cells, and the heterogeneity is the consequence of genomic instabilities such as chromosomal rearrangements, DNA mutations, and epigenetic changes [1]. Malignant tumors can invade the surrounding tissue and travel to distant parts of the body where they develop into secondary tumors (macrometastases) [2] It has been known for some time that metastases from certain tumors develop in certain organs. Ewing had a different opinion, and in 1928, he suggested that the anatomy and the vasculature control the metastases found in clinical practice [4]. Since both theories survived over time, the conclusion is that both ways can contribute to the affinity of cancer cells towards certain organs [5]. By secreting various growth factors, cells around the neoplasm fibroblasts, epithelial cells, and endothelial cells play roles in the activation of the tumor promoting pathways [7]
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