The Role of CD147 in the Invasiveness of Follicular Thyroid Carcinoma Cells

Omi, Yoko; Shibata, Noriyuki; Okamoto, Takahiro; Obara, Takao; Kobayashi, Makio

doi:10.1089/thy.2010.0426

Cited by 15 publications

(17 citation statements)

References 28 publications

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“…Enhanced EMMPRIN expression has been described before in many types of tumor tissues, but was usually not accompanied by detection of EMMPRIN expression on stromal cells (Zhong et al, 2008; Liang et al, 2009; Omi et al, 2012; Pinheiro et al, 2012; Lu et al, 2013), suggesting that stromal cell expression of EMMPRIN in vivo was very low and below the levels of antibody detection. Studies in vitro demonstrated that tumor cells enhance their expression of EMMPRIN when co-cultured with other cell types, such as fibroblasts (Tang et al, 2004; Sato et al, 2009) or endothelial cells (Caudroy et al, 2002; Bougaten et al, 2009), but expression of EMMPRIN in monocytes/macrophages co-cultured with tumor cells was hardly investigated.…”

Section: Discussionmentioning

confidence: 89%

Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN

Amit-Cohen¹,

Rahat²,

Rahat³

2013

Front. Physiol.

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Tumor macrophages are generally considered to be alternatively/M2 activated to induce secretion of pro-angiogenic factors such as VEGF and MMPs. EMMPRIN (CD147, basigin) is overexpressed in many tumor types, and has been shown to induce fibroblasts and endothelial cell expression of MMPs and VEGF. We first show that tumor cell interactions with macrophages resulted in increased expression of EMMPRIN and induction of MMP-9 and VEGF. Human A498 renal carcinoma or MCF-7 breast carcinoma cell lines were co-cultured with the U937 monocytic-like cell line in the presence of TNFα (1 ng/ml). Membranal EMMPRIN expression was increased in the co-cultures (by 3–4-folds, p < 0.01), as was the secretion of MMP-9 and VEGF (by 2–5-folds for both MMP-9 and VEGF, p < 0.01), relative to the single cultures with TNFα. Investigating the regulatory mechanisms, we show that EMMPRIN was post-translationally regulated by miR-146a, as no change was observed in the tumoral expression of EMMPRIN mRNA during co-culture, expression of miR-146a was increased and its neutralization by its antagomir inhibited EMMPRIN expression. The secretion of EMMPRIN was also enhanced (by 2–3-folds, p < 0.05, only in the A498 co-culture) via shedding off of the membranal protein by a serine protease that is yet to be identified, as demonstrated by the use of wide range protease inhibitors. Finally, soluble EMMPRIN enhanced monocytic secretion of MMP-9 and VEGF, as inhibition of its expression levels by neutralizing anti-EMMPRIN or siRNA in the tumor cells lead to subsequent decreased induction of these two pro-angiogenic proteins. These results reveal a mechanism whereby tumor cell-macrophage interactions promote angiogenesis via an EMMPRIN-mediated pathway.

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Section: Discussionmentioning

confidence: 89%

Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN

Amit-Cohen¹,

Rahat²,

Rahat³

2013

Front. Physiol.

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“…The functional importance of CD147 has been demonstrated to be associated with its ability to stimulate MMP expression. CD147 can induce the production of MMP-1, MMP-2, MMP-3, MMP-9, MMP-14, and MMP-15 (22). Supporting its key role in the processes of tumorigenesis and metastasis, CD147 has been reported to be one of the most constantly upregulated mRNAs in metastatic cells (23).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of CD147 by chitooligosaccharide inhibits MMP-2 expression and suppresses the metastatic potential of human gastric cancer

Luo

Xiao

et al. 2014

Oncology Letters

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Metastasis is considered to be the major cause of mortality in patients with cancer, and gastric cancer is a highly metastatic cancer. In the present study, the anti-metastatic activity of chitooligosaccharide (COS) in human gastric cancer cells and its underlying mechanism were investigated. It was found that COS significantly inhibited SGC-7901 cell proliferation and metastasis in a dose-dependent manner, as observed by MTT, wound-healing and Transwell assays. Quantitative real-time polymerase chain reaction and western blot analysis indicated that COS could decrease the expression of cluster of differentiation 147 (CD147) and subsequently reduce matrix metalloproteinase-2 (MMP-2) expression. A clear dose-dependent inhibition of MMP-2 activity was also observed in SGC-7901 cells following treatment with COS in gelatin zymography experiments. Furthermore, overexpression of CD147 (when transfected with pEGFP-C1 plasmid) in SGC-7901 cells partially protected against COS-induced inhibition of MMP-2. The results of the present study demonstrated the potential of COS in suppressing gastric cancer metastasis, and that the CD147/MMP-2 pathway may be involved as the key mechanism of its anti-metastatic effect.

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“…22 RNAi targeted CD147 reduced the invasive activity of follicular thyroid carcinoma and was associated with the down-regulation of MMP-2, MMP-3, MMP-7, and MMP-9. 23 The expression of CD147 in follicular thyroid carcinoma was promoted by epidermal growth factor, possibly via the phosphoinositol-3 kinase, extracellular signal-regulated protein kinase, or c-Jun N-terminal kinase pathway. 23 The signaling pathway used by CD147 to stimulate MMP remains unknown.…”

Section: Roles Of Cd147 In Ovarian Cancer Progression Including Lessmentioning

confidence: 96%

“…23 The expression of CD147 in follicular thyroid carcinoma was promoted by epidermal growth factor, possibly via the phosphoinositol-3 kinase, extracellular signal-regulated protein kinase, or c-Jun N-terminal kinase pathway. 23 The signaling pathway used by CD147 to stimulate MMP remains unknown. The p38 MAPK signaling pathway is believed to be involved.…”

Section: Roles Of Cd147 In Ovarian Cancer Progression Including Lessmentioning

confidence: 96%

CD147 in Ovarian and Other Cancers

Yang¹,

Chen²

2013

Int J Gynecol Cancer

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Ovarian cancer, a gynecological malignancy, is the most common cause of death in older women worldwide. The overall 5-year survival of ovarian cancer patients is only 20% because of late diagnosis, as well as distant metastasis and multidrug resistance. Therefore, predictive and prognostic markers are urgently required for the early diagnosis of ovarian cancer. CD147, an extracellular matrix metalloproteinase inducer, is overexpressed in ovarian cancers. Current knowledge suggests that CD147 is associated with the survival and progression of ovarian cancer, and is considered as a biomarker of poor outcome. Here, we specifically review the roles of CD147 in ovarian cancer progression and discuss the diagnostic and prognostic value of CD147 in patients with ovarian cancer. CD147 promotes ovarian cancer progression by its involvement in every facet of malignancy, including invasion, metastasis, survival, angiogenesis, and drug resistance. Although it is not fully confirmed, the combination of CD147 with other biomarkers might be of diagnostic value.

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The Role of CD147 in the Invasiveness of Follicular Thyroid Carcinoma Cells

Abstract: These results provide in vivo evidence for CD147 upregulation in FTC and in vitro evidence for EGF-stimulated CD147 induction via the PI3K, ERK, and JNK pathways. They suggest the involvement of CD147 in the invasiveness of FTC cells via regulation of MMPs.

Cited by 15 publications

References 28 publications

Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN

Tumor cell-macrophage interactions increase angiogenesis through secretion of EMMPRIN

Downregulation of CD147 by chitooligosaccharide inhibits MMP-2 expression and suppresses the metastatic potential of human gastric cancer

CD147 in Ovarian and Other Cancers

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