The role of EMMPRIN expression in ovarian epithelial carcinomas

Zhao, Yang; Chen, Shuo; Gou, Wenfeng; Niu, Zhe-Feng; Zhao, Shuang; Xiao, Ling; Takano, Yasuo; Zheng, Haixue

doi:10.4161/cc.25950

Cited by 25 publications

(22 citation statements)

References 52 publications

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“…Previous studies show that the treatment with baicalein decreases CD147 expression in SMMC‐7721 cells, accompanied by the occurrence of apoptosis and autophagy (Zhang et al, ). In ovarian epithelial carcinomas, CD147 small interfering RNA treatment induces apoptosis via downregulating anti‐apoptotic protein surviving (Zhao et al, ). In CHO‐CD147 cells, CD147 is found to inhibit apoptosis under methotrexate treatment (Zhao et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Grass et al (2013) determine that CD147 can activate EGFR-Ras-ERK signaling pathway, and the activation of Ras gene induces cell proliferation (Malumbres and Barbacid, 2003). In ovarian cancer, as a partner of monocarboxylate transporter 1, CD147 mediates cell proliferation by promoting VEGF and MMPs (Zhao et al, 2013a). Cyclin D1 is an important cyclin, which has been found to be overexpressed in proliferating cells.…”

Section: Discussionmentioning

confidence: 99%

“…Data are presented as mean AE SD (n ¼ 5); ÃÃ P < 0.01, ÃÃÃ P < 0.001. (Zhao et al, 2013a). In CHO-CD147 cells, CD147 is found to inhibit apoptosis under methotrexate treatment (Zhao et al, 2013b).…”

Section: Discussionmentioning

confidence: 99%

“…In hepatocellular carcinoma (HCC), CD147 overexpression promotes migration and invasion of tumors by promoting matrix metalloproteinase (MMP) production (Liao et al, ; Wu et al, ), regulating actin reorganization (Zhao et al, ), and inducing epithelial–mesenchymal transition (Wu et al, ). Some reports show that CD147 promotes cell proliferation in ovarian cancer (Zhao et al, ) and pancreatic cancer (Li et al, ) via activating vascular endothelial growth factor (VEGF), MMP‐9 secretion, and the ERK1/2 signaling pathway. However, most studies aim at the role of CD147 in tumor progression using tumor cell models.…”

Section: Introductionmentioning

confidence: 99%

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CD147 overexpression promotes tumorigenicity in Chinese hamster ovary cells

Yong

Liao

Ding

et al. 2016

Cell Biology International

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CD147 overexpresses in many epithelium-originated tumors and plays an important role in tumor migration and invasion. Most studies aim at the role of CD147 in tumor progression using tumor cell models. However, the influence of abnormal overexpression of CD147 on neoplastic transformation of normal cells is unknown. Here, the role of CD147 in malignant phenotype transformation in CHO cells was investigated. Three CHO cell lines that stably overexpressed CD147 (CHO-CD147), EGFP-CD147 (CHO-EGFP-CD147), and EGFP (CHO-EGFP) were generated by transfection of plasmids containing human CD147, EGFP-human CD147, and EGFP genes into CHO cells. Cell migration and invasion were detected by wound healing and transwell matrix penetration assay. Trypan blue exclusion, MTT, cell cycle analysis, and BrdU cell proliferation assay were used to detect cell viability and cell proliferation. Annexin V-FITC analysis was performed to detect apoptosis. We found that CD147 overexpression promoted the migration and invasion of CHO cells. CD147 accelerated the G1 to S phase transition and enhanced the CHO cell proliferation. Overexpression of CD147 inhibited both early- and late-stages of apoptosis of CHO-CD147 cells, which is caused by serum deprivation. CHO-EGFP-CD147 cells showed an increased anchorage-independent growth compared with CHO-EGFP cells as detected by soft-agar colony formation assay. The tumors formed by CHO-CD147 cells in nude mice were larger and coupled with higher expression of proliferating cell nuclear antigen and Ki-67 than that of CHO cells. In conclusion, human CD147 overexpression induces malignant phenotype in CHO cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

CD147 overexpression promotes tumorigenicity in Chinese hamster ovary cells

Yong

Liao

Ding

et al. 2016

Cell Biology International

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“…The role of CD147 in tumorigenesis is related to the inducement of MMP expression. It stimulates the secretion of MMPs from fibroblasts to degrade the basement membrane and the ECM, to facilitate cancer cell penetration, migration, metastasis, and angiogenesis (Weidle et al, 2010;Chen et al, 2012;Zhao et al, 2013). The degradation of the ECM and the cell adhesion contacts, and the formation of blood vessels, are the main events during metastasis that are initiated with CD147.…”

Section: Adhesion and Signal Moleculesmentioning

confidence: 99%

Glycosylation changes leading to the increase in size on the common core of N-glycans, required enzymes, and related cancer-associated proteins

Karaçalı¹,

İzzetoğlu²,

Deveci³

2014

Turk J Biol

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Glycan parts of glycoconjugates on the surfaces of cells regulate many kinds of interactions between the cells and their immediate environments. Alterations in glycosylation on the cancer-associated glycoproteins are responsible for changes in their molecular interactions and biological functions. Glycosylation changes occur in the core and/or at the nonreducing end of the oligosaccharide chains of N-glycans. In this review, we focus on the branching of the common core structure of N-glycans, the responsible enzyme, and the extensions of some of the branches causing size increases on the surface of tumor cells. Abnormal branching, elongation of the branches, and increasing size of the common core of N-glycans are the typical features of these changes and are related with malignant transformations. Seven N-acetylglucosaminyltransferases (GnTs) (GnT-I, GnT-II, GnT-III, GnT-IV, GnT-V, GnT-VI, and GnT-IX) and α1,6-fucosyltransferase (FUT8) initiate the new branches on the core. GnT-IV, GnT-V, and GnT-IX initiate the branches available for poly-LacNAc extensions, which are responsible for tumor progression and metastasis. GnT-III prevents the catalytic activity of GnT-II, GnT-IV, GnT-V, and FUT8 to form branching and elongation of the branches. The contributions of GnT-III and the other enzymes to the cancer progression are in conflict with each other. While GnT-III prevents cancer, the others increase metastasis. The function of FUT8 is related to signal transduction and its activity is higher in tumor tissue than in healthy tissue. The impact of glycosylation changes on some of the cancer-associated proteins (growth factor receptors, adhesion and signal molecules, CD147, TIMP-1, and matriptase) is also summarized.

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Cell expression patterns of CD147 in N-diethylnitrosamine/phenobarbital-induced mouse hepatocellular carcinoma

Meng

et al. 2014

J Mol Hist

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Overexpression of CD147/basigin in hepatic cells promotes the progression of hepatocellular carcinoma (HCC). Whether CD147 also expressed in liver non-parenchymal cells and associated with HCC development was unknown. The aim of the study was to explore time-dependent cell expression patterns of CD147 in a widely accepted N-diethylnitrosamine/phenobarbital (DEN/PB)-induced HCC mouse model. Liver samples collected at month 1-12 of post-DEN/PB administration were assessed the localization of CD147 in hepatocytes, endothelial cells, hepatic stellate cells, and macrophages. Immunohistochemistry analysis showed that CD147 was upregulated in liver tumors during month 1-8 of DEN/PB induction. Expression of CD147 was positively correlated with cytokeratin 18, a hepatocyte marker (r = 0.7857, P = 0.0279), CD31 (r = 0.9048, P = 0.0046), an endothelial cell marker, and CD68, a macrophage marker (r = 0.7619, P = 0.0368). A significant correlation was also observed between CD147 and alpha-smooth muscle actin (r = 0.8857, P = 0.0333) at DEN/PB initiation and early stage of tumor formation. Immunofluorescence and fluorescence in situ hybridization showed that CD147 co-expressed with cytokeratin 18, CD31, alpha-smooth muscle actin, and CD68. Moreover, there existed positive correlations between CD147 and microvessel density (r = 0.7857, P = 0.0279), CD147 and Ki-67 (r = 0.9341, P = 0.0022) in the development of DEN/PB-induced HCC. In conclusion, our results demonstrated that CD147 was upregulated in the liver parenchymal and mesenchymal cells and involved in angiogenesis and tumor cell proliferation in the development of DEN/PB-induced HCC.

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The role of EMMPRIN expression in ovarian epithelial carcinomas

Cited by 25 publications

References 52 publications

CD147 overexpression promotes tumorigenicity in Chinese hamster ovary cells

CD147 overexpression promotes tumorigenicity in Chinese hamster ovary cells

Glycosylation changes leading to the increase in size on the common core of N-glycans, required enzymes, and related cancer-associated proteins

Cell expression patterns of CD147 in N-diethylnitrosamine/phenobarbital-induced mouse hepatocellular carcinoma

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