Abstract
Metastasis is one of the characteristics of malignant tumors and the main cause of death worldwide. The process of metastasis is mainly affected by tumor metastasis genes, tumor metastasis suppressor genes, tumor microenvironment, extracellular matrix degradation, and other factors. Thus, it is essential to elucidate the mechanism of metastasis and find the therapeutic targets in order to prevent the development of malignant tumors. KAI1/CD82, a member of tetraspanin superfamily of glycoproteins, has been reported as a tumor metastasis suppressor gene in various types of cancers without affecting the tumor formation. Many studies have demonstrated that low expression of KAI1/CD82 might lead to poor prognosis due to its interactions with other tetraspanins and integrins, resulting in the regulation of cell motility and invasion, cell-cell adhesion, and apoptosis. Considering its pathological and physiological significance, KAI1/CD82 could be a potential strategy for clinical predicting and preventing tumor progression and metastasis. The present review aims to discuss the role of KAI1/CD82 in metastasis for different cancers and examine its prospects as a metastasis biomarker and a therapeutic target.
Highlights
Metastasis has been the leading cause of cancer-related mortality
A recent study revealed a positive correlation between CD82 and BCL2L12 expression at mRNA and protein levels due to STAT5A and AKT signaling in Acute myelogenous leukemia (AML) cells isolated from patients, which eventually stimulated proliferation and engrafting of leukemia cells [74]
E KAI1/CD82 mRNA expression level was significantly higher in the patients with acute lymphoblastic leukemia (ALL)-ND, B-cell-ALL, and T-cell-ALL compared with those aged match children without bone marrow (BM) disease [78]
Summary
Metastasis has been the leading cause of cancer-related mortality. It is well known that tumor metastasis refers to the process in which malignant tumor cells leave the primary site, pass through vessels and enter blood circulation and lymphatic circulation of the host, and eventually form malignant tumor, the same type of tumor as the primary one [1, 2]. Despite the clinically therapeutic progress of hepatocellular carcinoma (HCC) such as liver surgical resection, transplantation, or chemotherapy, the survival rate was less than 5% within five years, mainly due to the high rate of postoperative recurrence and metastasis after surgical resection [16, 17] It is well-known that the KAI1/CD82 mRNA and protein expression was significantly reduced in the tumors compared to adjacent nontumor liver tissues obtained from the same patient [18]. A present study suggests that KAI1/CD82 functions in suppressing TGF-β1- and Wnt-induced EMT in prostate cancer cells by inhibiting the TGF-β1/Smad and Wnt/β-catenin pathways, resulting in the development of a motile and invasive mesenchymal phenotype related to the initiation of the metastatic cascade [11].
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