To determine the effects of EMMPRIN-2 on head and neck cancer progression, we transfected head and neck cancer cells with an EMMPRIN-2 expression vector and EMMPRIN-2 siRNA to exogenously modulate EMMPRIN-2 expression and examined the functional importance of EMMPRIN-2 in head and neck cancer invasion and metastasis.
HAb18G/CD147 belongs to the immunoglobulin superfamily and predominantly functions as an inducer of matrix metalloproteinase secretion for tumor invasion and metastasis.
In this study, we demonstrated that CD147 was overexpressed in breast cancer tissues and cell lines, and the high expression correlated with tumor invasion and metastasis.
CD147 has been proved to be enriched on the surface of many tumor cells, promoting tumor growth, invasion and metastasis by its stimulation effect on adjacent fibroblasts to produce matrix metalloproteinases.
EMMPRIN, a transmembrane glycoprotein known to promote survival, invasion and metastasis of tumor cells through multiple pathways and mechanisms, has been found to be overexpressed in various types of cancer cells.
The correlation of the expression of MMP9 and CD147 with invasion and metastasis of invasive squamous cell carcinoma (SCC) of the uterine cervix has not been examined.
In this study, we demonstrate that the endoplasmic reticulum (ER)-associated protein calcium-modulating cyclophilin ligand (CAML) is bound to Basigin, a widely expressed integral plasma membrane glycoprotein and extracellular matrix metalloproteinase inducer (EMMPRIN, or CD147) implicated in melanoma proliferation, invasiveness, and metastasis.
To define the role of CD147 in invasion and metastasis more precisely, we utilized gene silencing to inhibit the expression of CD147 in pancreatic cancer cells.
Extracellular matrix metalloproteinase inducer (EMMPRIN) was reported to involve in the invasion and metastasis of malignancies by regulating the expression of vascular endothelial growth factor (VEGF) in stromal and cancer cells.
CD147 (EMMPRIN or basigin) is a leading gene relating to hepatocarcinogenesis and metastasis, and is detected in transmembrane, exosome or circulating forms in HCC patients.
<b>Conclusions</b>: The <i>in vitro</i> and <i>in vivo</i> study demonstrated dual effects of Metuzumab in effectively mediating ADCC by activating effector cells, and inhibiting metastasis of esophageal cancer through blockade the function of CD147, providing justification for moving Metuzumab forward to clinical development in esophageal cancer.
Soluble EMMPRIN in turn acts in a paracrine fashion on stroma cells that are both adjacent and distant to tumor sites to further stimulate the production of MMPs and additional EMMPRIN, which consequently contributes to tumor angiogenesis, tumor growth, and metastasis.
Accumulating evidences have shown that CD147 is over-expressed in various tumors, including melanoma, liver cancer, and lung cancer, and orchestrates tumor cell proliferation, apoptosis, invasion and metastasis, multidrug resistance and glycolysis through critical molecules such as MMPs, MCTs, Caveolin-1, and VEGF.
In a concentration‑dependent manner, emodin inhibited the TRAF6/HIF‑1α/VEGF and TRAF6/CD147/MMP9 signaling pathways to suppress angiogenesis and metastasis.
HAb18G/CD147, a transmembrane glycoprotein highly expressed in various types of malignant cells, mainly functions as an inducer of matrix metalloproteinases to promote tumor growth, invasion and metastasis.
From our data we conclude that hypo-phosphorylated CD147 promotes the migration and invasion of HCC cells and correlates with an unfavorable prognosis in HCC patients, indicating that targeting the aberrantly hypo-phosphorylated form of CD147 may be instrumental for the development of novel therapeutic modalities directed against HCC metastasis.