Since the transforming growth factor β (TGF-β) and Wnt signals induce EMT in various epithelial cell types, we examined whether and how the CD82/KAI1metastasis suppressor affects the TGF-β and Wnt signal-dependent EMT in human prostate cancer cells.
There was a significant negative correlation between CD82 expression in tissues and CD82 content in exosomes, which indicated that CD82 expression was redistributed from tissues to the blood with the development and metastasis of breast cancer.
The tetraspanin CD82 is a potent suppressor of tumor metastasis and regulates several processes including signal transduction, cell adhesion, motility, and aggregation.
In multivariate analysis, high VM, Notch4, DLL4 levels, tumor size, LNM, DM, TNM stage, and low KAI1/CD82 levels were potential to be independent prognostic factors for overall survival time (OST) in NSCLC patients.VM and the expression of Notch4, DLL4, and KAI1/CD82 represent promising markers for tumor metastasis and prognosis, and maybe potential therapeutic targets for NSCLC.
Vasculogenic mimicry (VM, new blood supply formation in malignant tumors), E-Cadherin (a calcium-dependent transmembrane glycoprotein that mediates intercellular adhesion), KAI1 (a suppressor gene of tumor metastasis) are all valuable factors for metastasis and prognosis in diverse common human cancers.
Of the tetraspanin proteins, CD82 has been shown to promote homotypic cell-cell adhesion, which partially accounts for its role in suppressing cancer invasion and metastasis.
The purpose of this study was to investigate the role of intravenously administered KAI1/CD82 genetically transduced EPCs in the tumorigenesis and metastasis of nasopharyngeal carcinoma (NPC).
Importantly, we show that in all these cancer cells liprin-α1 knockdown leads to the upregulation of transmembrane protein CD82, which is a suppressor of metastasis in several solid tumors.
In RA-synovium, CD82 was expressed in RASF close to blood vessels, LL, sites of cartilage invasion and colocalised with distinct integrins involved in tumour metastasis suppression but also in RA-synovium by RASF.
MiR-338-5p mimics improved the growth and metastasis of A375 cells transfected with CD82 vector, while inhibition of miR-338-5p attenuated the pro-tumor function of si-CD82 in A375 cells.
Our findings suggest that splicing of KAI1 does not only abrogate its tumor suppressive functions, but even more, promotes tumor biological effects in favor of cancer progression and metastasis.
This novel finding will improve our understanding of the mechanism by which CD82 inhibits metastasis, and suggested that EC1 mimic peptide may be a promising candidate for developing anti-metastasis drugs.
Taken together, CD82 played a prominent role in migration and invasion of RCC cells and it might exhibit its inhibitory role in RCC metastasis via block TGF-β1/Smad signaling pathway.
KAI1 may be involved in retinoblastoma metastasis, and increased expression of KAI1 significantly inhibits the metastatic ability of RB cells <i>in vitro</i>.
In this review, we focus on the differential expression of KAI1/CD82, a tumor metastasis suppressor gene that can inhibit cancer invasion and cell metastasis during NSCLC.
Here we have identified and characterized a primarily nuclear non-polyadenylated, antisense (as)-lncRNA, initiating upstream of the KAI1 human metastasis suppressor gene transcription start site; and elongating in the opposite direction to KAI1 mRNA.
Here, by using mass spectrometry, bioinformatics analysis and luciferase reporter assay, we showed that miR-K6-5p directly targeted the coding sequence of CD82 molecule (CD82), a metastasis suppressor.
Vasculogenic mimicry (VM, blood supply formation often seen in highly aggressive tumors), Aldehyde dehydrogenase 1 (ALDH1, a biomarker of cancer stem cells), KAI1 (a suppressor gene of tumor metastasis) are all valuable factors for metastasis and prognosis in diverse human cancers.