Home Neoplasma 2018 Neoplasma Vol.65, No.6, p.823-839, 2018

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Neoplasma Vol.65, No.6, p.823-839, 2018

Title: ADAM protein family – its role in tumorigenesis, mechanisms of chemoresistance and potential as diagnostic and prognostic factors
Author: L. Zadka, M. J. Kulus, K. Piatek

Abstract: ADAMs are a family of transmembrane proteins described for the first time in the 1990’s. ADAMs is an abbreviation of “A Disintegrin and Metallo-proteinases”. Their earliest known role was involvement in gamete fusion, and their adhesion properties in intercellular interactions also suggested involvement in tumor biology. Further research emphasized the importance of ADAM proteins in the regulation of neoplastic processes due to their influence on adhesion, cell migration, proteolysis and cell signaling. Variable ADAM expression in cancer and normal tissue was the basis for considering these proteins as diagnostic markers. Recent numerous studies have been published suggesting the prognostic value of this protein family members. The ADAMs transmembrane proteins regulate processes associated with carcinogenesis and neoplastic progression, including immune response evasion, growth induction and metastasis. Proteolysis and shedding of membrane proteins and binding integrins by ADAMs lead to the activation of numerous growth factors, changes in the extracellular matrix, adhesion proteins and angiogenesis. ADAMs potential as prognostic and diagnostic markers in cancer treatment is a particularly interesting issue and has great practical significance. There are many new studies concerning ADAMs’ roles in carcinogenesis, but there are no recent reviews of the latest developments in this field.
The aim of this systematic review is to analyze the results of studies published on ADAMs in the last 5 years, to present their roles in neoplasm pathogenesis and their potential utility in clinical oncology.

Keywords: ADAM, cancer, metalloproteases, sheddases
Published online: 08-Oct-2018
Year: 2018, Volume: 65, Issue: 6 Page From: 823, Page To: 839

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