The roles of CD147 in the progression of gliomas

Fei, Fei; Li, Sanzhong; Zhou, Fei; Chen, Zhi‐Nan

doi:10.1586/14737140.2015.1092874

Cited by 12 publications

(13 citation statements)

References 97 publications

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“…A number of studies have demonstrated that CD147 serves an important role in glioma (15,27). The results of the present study also proved that CD147 was able to affect the development of glioma cells; knockdown of CD147 inhibited glioma cell growth, whereas CD147 overexpression enhanced cell growth in glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Shikonin inhibits proliferation and induces apoptosis in glioma cells via downregulation of CD147

et al. 2019

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Shikonin, a traditional Chinese medicine, has been identified as being capable of inducing apoptosis in various tumors, including glioma, and is thus considered to be a promising therapeutic agent for tumor therapy. However, little is known about the molecular mechanism of shikonin in glioma. The present study investigated the influence of shikonin on the proliferation and apoptosis of glioma cells U251 and U87MG and explored the potential molecular mechanisms. It was identified that shikonin was able to induce apoptosis in human glioma cells in a time- and dose-dependent manner, and a decreased expression level of cluster of differentiation (CD)147 was observed in shikonin-treated U251 and U87MG cells. Knockdown of CD147 inhibited U251 and U87MG cell growth, whereas CD147 overexpression enhanced cell growth and decreased shikonin-induced apoptosis. Additionally, an increased expression level of CD147 suppressed the elevated production of reactive oxygen species and mitochondrial membrane potential levels induced by shikonin. The data indicated that shikonin-induced apoptosis in glioma cells was associated with the downregulation of CD147 and the upregulation of oxidative stress. CD147 may be an optional target of shikonin-induced cell apoptosis in glioma cells.

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Section: Discussionmentioning

confidence: 99%

Shikonin inhibits proliferation and induces apoptosis in glioma cells via downregulation of CD147

et al. 2019

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“…N ‐acetylglucosaminyltransferase (GnT)‐V is a key glycosyltransferase that regulates the formation of β1,6‐Glc N Ac ( N ‐acetylglucosamine) branches during N‐glycosylation, which modulates the conversion of LG‐EMMPRIN to HG‐EMMPRIN . The glycosylation of EMMPRIN is of great importance in various physiological processes and pathological progression, such as human parturition, atherosclerotic lesions, inflammatory activity, tumor metastasis and chemoresistance . Furthermore, in the tumor microenvironment, EMMPRIN on tumor cells stimulates the expression of several types of MMPs through crosstalk with fibroblasts .…”

Section: Introductionmentioning

confidence: 99%

The role of extracellular matrix metalloproteinase inducer glycosylation in regulating matrix metalloproteinases in periodontitis

Zhang

Yang

Zhang

et al. 2018

J of Periodontal Research

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We conclude that EMMPRIN glycosylation participates in the regulation of MMP-2 and MMP-9 production through mediating the interaction of HIOECs and HGFs. Inhibiting EMMPRIN glycosylation can reduce the activation of MMP-2 and MMP-9 and suppress the degradation of extracellular matrix (ECM) in the HIOEC/HGF co-culture model. Therefore, this study suggests that EMMPRIN glycosylation may affect the host immune-inflammatory response by regulating MMPs in periodontitis.

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“…EMMPRIN has been demonstrated to be associated with the degree of malignancy, metastasis and prognosis of different types of cancer ( 35 , 36 ). The upregulation of EMMPRIN has also been described as a biomarker for a poor prognosis in patients with glioma ( 37 ). Sameshima et al ( 38 ) revealed that EMMPRIN was only expressed by the vascular endothelium in normal brain tissues, but was distributed throughout the cell membrane and cytoplasm in glioma tissues.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of EMMPRIN by microRNA‑124 suppresses the growth, invasion and tumorigenicity of gliomas

et al. 2021

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MicroRNAs (miR) are a group of non-coding, small RNAs, 18-20 nucleotides in length, that are frequently involved in the development of a variety of different types of cancer, including glioma, which is a type of severe tumor in the brain. Previous studies reported that miR-124 levels were downregulated in glioma specimens; however, the potential role of miR-124 in glioma currently remains unclear. The present study performed experiments, including dual-luciferase reporter assay (DLRA), MTT assay, transwell assay and flow cytometry, with the aim of elucidating the molecular mechanism of miR-124 in glioma. The results indicated that miR-124 expression was decreased in glioma tissues, accompanied by the increased expression of extracellular matrix metalloproteinase inducer (EMMPRIN). The expression of EMMPRIN was inhibited by miR-124 transfection. The DLRA results revealed that EMMPRIN directly targets miR-124. Furthermore, upon overexpression of miR-124 in the U87 cells, cell proliferation was significantly inhibited, apoptosis was increased, and cell migration and invasion were decreased. Furthermore, tumor growth was blocked by miR-124 in mice. Based on these results, the present study concluded that miR-124 is critical for amelioration of glioma by targeting EMMPRIN, thereby acting as a tumor suppressor. Thus, miR-124/EMMPRIN constitutes a plausible basis for the treatment of glioma.

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The roles of CD147 in the progression of gliomas

Cited by 12 publications

References 97 publications

Shikonin inhibits proliferation and induces apoptosis in glioma cells via downregulation of CD147

Shikonin inhibits proliferation and induces apoptosis in glioma cells via downregulation of CD147

The role of extracellular matrix metalloproteinase inducer glycosylation in regulating matrix metalloproteinases in periodontitis

Inhibition of EMMPRIN by microRNA‑124 suppresses the growth, invasion and tumorigenicity of gliomas

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