Acquisition of anoikis resistance through CD147 upregulation: A new mechanism underlying metastasis of hepatocellular carcinoma cells

Ke, Xia; Li, Ling; Dong, Honglin; Chen, Zhi‐Nan

doi:10.3892/ol.2012.658

Cited by 26 publications

(25 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous findings have indicated that CD147 expression protects breast cancer cells from anoikis, at least in part, by a mitogen-activated protein kinase-dependent reduction of Bim, which is a proapoptotic BH3-only protein, and that knockdown of CD147 expression by RNA interference sensitized cancer cells to anoikis through the activation of caspase-3 [ 52 ]. Ke et al found that CD147 expression was significantly higher in hepatocellular carcinoma cells (SMMC-7721) resistant to anoikis compared with the parental cells, and that CD147 knockdown by siRNA also remarkably induced cell anoikis, partially via inactivation of the PI3K/Akt signaling pathway [ 53 ]. In summary, the acquisition of anoikis resistance through upregulation of CD147 may represent a newly recognized mechanism underlying the metastasis of malignant tumor cells.…”

Section: Cd147 In Tumorsmentioning

confidence: 99%

The altered glucose metabolism in tumor and a tumor acidic microenvironment associated with extracellular matrix metalloproteinase inducer and monocarboxylate transporters

Dong

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Extracellular matrix metalloproteinase inducer, also knowns as cluster of differentiation 147 (CD147) or basigin, is a widely distributed cell surface glycoprotein that is involved in numerous physiological and pathological functions, especially in tumor invasion and metastasis. Monocarboxylate transporters (MCTs) catalyze the proton-linked transport of monocarboxylates such as L-lactate across the plasma membrane to preserve the intracellular pH and maintain cell homeostasis. As a chaperone to some MCT isoforms, CD147 overexpression significantly contributes to the metabolic transformation of tumor. This overexpression is characterized by accelerated aerobic glycolysis and lactate efflux, and it eventually provides the tumor cells with a metabolic advantage and an invasive phenotype in the acidic tumor microenvironment. This review highlights the roles of CD147 and MCTs in tumor cell metabolism and the associated molecular mechanisms. The regulation of CD147 and MCTs may prove to be with a therapeutic potential for tumors through the metabolic modification of the tumor microenvironment.

show abstract

Section: Cd147 In Tumorsmentioning

confidence: 99%

The altered glucose metabolism in tumor and a tumor acidic microenvironment associated with extracellular matrix metalloproteinase inducer and monocarboxylate transporters

Dong

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…Increased expression of CD147 was shown to correlate with enhanced tumor progression and poor prognosis in different cancers [ 6 – 8 ]. Thus, an attractive way to curb tumor progression is through suppression of the CD147-dependent cell proliferation, invasion and metastasis by RNAi-mediated silencing [ 5 , 9 ] and eventually induce cell apoptosis due to detachment of anchorage-dependent cell from the surrounding extracellular matrix [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Combination of VP3 and CD147-knockdown enhance apoptosis and tumor growth delay index in colorectal tumor allograft

et al. 2016

View full text Add to dashboard Cite

BackgroundCancer therapies that kill cancer cells without affecting normal cells is the ultimate mode of treating cancers. The VP3, an avian virus-derived protein, can specifically initiate cell death through several signal transduction pathways leading to apoptosis. In cancer, chemoresistance and cell survivability implicate the cell surface protein, CD147.MethodsIn this study, transfection of VP3 and silencing of CD147 genes was achieved through the treatment of tumors with pVIVO1-GFP/VP3 (VP3), psiRNA-CD147/2 (shCD147/2), and their combination of CT26 colon cancer cell-induced in mice. The effectiveness of tumor-treatment was ascertained by electrophoresis, TUNEL assay, and flow cytometry analysis. While histopathological and biochemical analysis were used as toxic side effect identification.ResultsThe tumor growth delay index (TGDI) after treatment with VP3, shCD147/2, and their combination treatments increased by 1.3-, 1.2-, 2.0- and 2.3-fold respectively, over untreated control. The VP3-shCD147/2 combination treatment was more efficacious then either VP3 or shCD147/2 alone in the retardation of mouse CT26 colorectal cell tumor allograft.ConclusionThe antitumor effect of the combination treatment is the result of synergistic effects of VP3 and shCD147/2 on the tumor cells resulting in apoptosis. Thus, the study shows that combination of VP3 and shCD147/2 treatment can be developed into a potential approach for anticolorectal cancer treatment regimen.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2530-8) contains supplementary material, which is available to authorized users.

show abstract

“…These results suggest that HAb18G/CD147 pay an important role in cancer metastasis and progression. Recently, we showed that HAb18G/CD147 promote epithelial-mesenchymal transition (21), anoikis resistance and anchorage-independent growth in vitro (22, 23) and tumorigenic potential of liver cancer in vivo (21), indicating a possible role of HAb18G/CD147 in tumor initiation.…”

Section: Introductionmentioning

confidence: 99%

HAb18G/CD147 Promotes pSTAT3-Mediated Pancreatic Cancer Development via CD44s

Tang

et al. 2013

Clinical Cancer Research

Self Cite

View full text Add to dashboard Cite

Purpose STAT3 plays a critical role in initiation and progression of pancreatic cancer. However, therapeutically targeting STAT3 is failure in clinic. We previously identified HAb18G/CD147 as an effective target for cancer treatment. In this study, we aimed to investigate potential role of HAb18G/CD147 in STAT3-involved pancreatic tumorigenesis in vitro and in vivo. Experimental Design The expression of HAb18G/CD147, pSTAT3 and CD44s were determined in tissue microarrays. The tumorigenic function and molecular signaling mechanism of HAb18G/CD147 was assessed by in vitro cellular and clonogenic growth, reporter assay, immunoblot, immunofluorescence staining, immunoprecipitation, and in vivo tumor formationusing loss or gain-of-function strategies. Results Highly expressed HAb18G/CD147 promoted cellular and clonogenic growth in vitro and tumorigenicity in vivo. CyPA, a ligand of CD147, stimulated STAT3 phosphorylation and its downstream genes cyclin D1/survivin through HAb18G/CD147 dependent mechanisms. HAb18G/CD147 was associated and co-localized with cancer stem cell marker CD44s in lipid rafts. The inhibitors of STAT3 and survivin, as well as CD44s neutralizing antibodies suppressed the HAb18G/CD147-induced cell growth. High HAb18G/CD147 expression in pancreatic cancer was significantly correlated with the poor tumor differentiation, and the high co-expression of HAb18G/CD147-CD44s-STAT3 associated with poor survival of patients with pancreatic cancer. Conclusions We identified HAb18G/CD147 as a novel upstream activator of STAT3 via interacts with CD44s and plays a critical role in the development of pancreatic cancer. The data suggest HAb18G/CD147 could be a promising therapeutic target for highly aggressive pancreatic cancer and a surrogate marker in the STAT3-targeted molecular therapies.

show abstract

Acquisition of anoikis resistance through CD147 upregulation: A new mechanism underlying metastasis of hepatocellular carcinoma cells

Cited by 26 publications

References 33 publications

The altered glucose metabolism in tumor and a tumor acidic microenvironment associated with extracellular matrix metalloproteinase inducer and monocarboxylate transporters

The altered glucose metabolism in tumor and a tumor acidic microenvironment associated with extracellular matrix metalloproteinase inducer and monocarboxylate transporters

Combination of VP3 and CD147-knockdown enhance apoptosis and tumor growth delay index in colorectal tumor allograft

HAb18G/CD147 Promotes pSTAT3-Mediated Pancreatic Cancer Development via CD44s

Contact Info

Product

Resources

About