The role of osteopontin in oral cancer: A brief review with emphasis on clinical applications

Osteopontin (OPN) is a calcium‐binding glycol‐phosphoprotein present in many physiologic and pathological processes. This protein can control bone cell adhesion, osteoclastic activity, and bone matrix mineralization. However, its participation in pathological processes such as atherosclerosis, sarco...

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Published in:Oral diseases 2022-03, Vol.28 (2), p.326-335
Main Authors: Santos, Erison Santana, Ramos, Joab Cabral, Roza, Ana Luiza Oliveira Corrêa, Mariz, Bruno Augusto Linhares Almeida, Paes Leme, Adriana Franco
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Angiogenesis
Arteriosclerosis
biomarkers
Bone matrix
carcinogenesis
Cell activation
Cell adhesion
Cell Line, Tumor
Cell proliferation
Cell Proliferation - genetics
extracellular matrix proteins
Humans
Metastases
Mineralization
Mouth Neoplasms
Oral cancer
oral squamous cell carcinoma
Osteoclasts
Osteopontin
Osteopontin - genetics
Phenotypes
Phosphatidylinositol 3-Kinases - metabolism
Sarcoidosis
Squamous cell carcinoma
TOR protein
Tuberculosis
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Summary:Osteopontin (OPN) is a calcium‐binding glycol‐phosphoprotein present in many physiologic and pathological processes. This protein can control bone cell adhesion, osteoclastic activity, and bone matrix mineralization. However, its participation in pathological processes such as atherosclerosis, sarcoidosis, tuberculosis, and cancer have been described. Some studies have shown that OPN may participate in the development and progression of oral cancer. Although the role of OPN in oral cancer is not fully understood, some studies have suggested that this protein may induce malignant phenotype of cells by activation of PI3K/AKT/mTOR pathway, which favors cell proliferation, invasion, metastasis, angiogenesis, and failure of treatment. This review discusses the possible mechanism of involvement of OPN in oral cancer and its potential clinical application in diagnosis and prognosis.
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.13716