Inhibition of CD147 Gene Expression via RNA Interference Reduces Tumor Cell Proliferation, Activation, Adhesion, and Migration Activity in the Human Jurkat T-Lymphoma Cell Line

Chen, Xiang; Su, Juan; Chang, Jing; Kanekura, Takuro; Li, Ji; Kuang, Ye; Peng, Sheng; Yang, Fang; Lü, Hui; Zhang, Jiang Lin

doi:10.1080/07357900701867892

Cited by 28 publications

(26 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…34 Bone marrow-derived cells are involved in the pathogenesis of PH. 13,14,35 Therefore, we hypothesized that Bsg deficiency in bone marrow-derived cells may impair hypoxia-induced PH in Bsg +/-mice.…”

Section: Vascular Bsg Is Essential For Hypoxia-induced Phmentioning

confidence: 99%

Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Satoh

Kikuchi

et al. 2014

Circulation Research

103

View full text Add to dashboard Cite

Section: Vascular Bsg Is Essential For Hypoxia-induced Phmentioning

confidence: 99%

Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Satoh

Kikuchi

et al. 2014

Circulation Research

103

View full text Add to dashboard Cite

“…Tumor cell migration is likely to be a crucial event for the progression of tumor invasion and metastasis (17,18). Recent reports have also revealed that the augmented expression of EMMPRIN directly or indirectly stimulates tumor cell migration in vitro (19,20). In addition, the interaction between EMMPRIN and membrane-associated molecules such as caveolin and annexin II on the cell surface has been reported to facilitate human carcinoma cell migration (21,22).…”

Section: Introductionmentioning

confidence: 99%

A novel functional site of extracellular matrix metalloproteinase inducer (EMMPRIN) that limits the migration of human uterine cervical carcinoma cells

Sato

Watanabe²,

Hashimoto³

et al. 2011

Int J Oncol

View full text Add to dashboard Cite

Abstract. EMMPRIN (extracellular matrix metalloproteinase inducer)/CD147, a membrane-bound glycoprotein with two extracellular loop domains (termed loops I and II), progresses tumor invasion and metastasis by increasing the production of matrix metalloproteinase (MMP) in peritumoral stoma cells. EMMPRIN has also been associated with the control of migration activity in some tumor cells, but little is known about how EMMPRIN regulates tumor cell migration. In the present study, EMMPRIN siRNA suppressed the gene expression and production of EMMPRIN in human uterine cervical carcinoma SKG-II cells. An in vitro scratch wound assay showed enhancement of migration of EMMPRIN-knockdown SKG-II cells. In addition, the SKG-II cell migration was augmented by adding an E. coli-expressed human EMMPRIN mutant with two extracellular loop domains (eEMP-I/II), which bound to the cell surface of SKG-II cells. However, eEMP-I/II suppressed the native EMMPRIN-mediated augmentation of proMMP-1/procollagenase-1 production in a co-culture of the SKG-II cells and human uterine cervical fibroblasts, indicating that the augmentation of SKG-II cell migration resulted from the interference of native EMMPRIN functions by eEMP-I/ II on the cell surface. Furthermore, a systematic peptide screening method using nine synthetic EMMPRIN peptides coding the loop I and II domains (termed EM1-9) revealed that EM9 ( 170 HIENLNMEADPGQYR 184 ) facilitated SKG-II cell migration. Moreover, SKG-II cell migration was enhanced by administration of an antibody against EM9, but not EM1 which is a crucial site for the MMP inducible activity of EMMPRIN. Therefore, these results provide novel evidence that EMMPRIN on the cell surface limits the cell migration of human uterine cervical carcinoma cells through 170 HIENLNMEADPGQYR 184 in the loop II domain. Finally, these results should provide an increased understanding of the functions of EMMPRIN in malignant cervical carcinoma cells, and could contribute to the development of clinical strategies for cervical cancer therapy.

show abstract

“…A pathogenic role for EMMPRIN in the inflammatory cascades in MS is suggested by its functions in regulating T cell activation and proliferation (5-7), and by the reports that EMMPRIN promotes the migration (8, 9), adhesion (10,11), and barrier-crossing properties (12, 13) of leukocytes. In support, inflammatory perivascular cuffs in the CNS of EAE and MS specimens have highly elevated EMMPRIN expression in many leukocyte subsets (11), and mice treated with anti-EMMPRIN Abs have reduced EAE clinical severity (12,20).…”

Section: Discussionmentioning

confidence: 99%

“…MS is an immune-mediated disorder of the CNS characterized by the generation of myelin-reactive T cells, demyelination, and axonal degeneration. Accumulating evidence supports functional roles for EMMPRIN during T cell activation and proliferation (5-7), migration (8,9), adhesion (10,11), and invasion (12,13), all steps important in the pathogenesis of MS as well as other immunological diseases (1). Although it is unclear how all these mechanisms connect, it is supported by the identification of several EMMPRIN-interacting proteins that correspond to these functions such as monocarboxylate transporters (MCTs) (14,15), integrins (16), CD98 (17), cyclophilins (18), and EMMPRIN itself (1,19).…”

mentioning

confidence: 99%

Impact of Minocycline on Extracellular Matrix Metalloproteinase Inducer, a Factor Implicated in Multiple Sclerosis Immunopathogenesis

Hahn

Kaushik

Mishra

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

Extracellular matrix metalloproteinase inducer (EMMPRIN, CD147) is a transmembrane glycoprotein that is upregulated on leukocytes in active lesions in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Administration of anti-EMMPRIN Abs reduces the severity of EAE. Minocycline is a tetracycline antibiotic with immune-modulatory properties that decreases the severity of EAE; it was recently found to attenuate the conversion from a first demyelinating event to clinically definite MS in a phase III trial. We investigated whether and how minocycline affects the expression of EMMPRIN on T cells in culture and in mice afflicted with EAE. EMMPRIN expression in cultures of mouse splenocytes or human PBMCs was elevated upon polyclonal T cell activation, and this was reduced by minocycline correspondent with decreased P-Akt levels. An established MS medication, IFN-β, also diminished EMMPRIN levels on human cells whereas this was not readily observed for fingolimod or monomethylfumarate. In EAE-afflicted mice, minocycline treatment significantly reduced EMMPRIN levels on splenic lymphocytes at the presymptomatic (day 7) phase, and prevented the development of disease. Day 7 spleen transcripts from minocycline-treated EAE mice had a significantly lower MMP-9/TIMP-1 ratio, and significantly lower MCT-1 and CD98 levels, factors associated with EMMPRIN function. Day 16 (peak clinical severity) CNS samples from EAE mice had prominent representation of inflammatory perivascular cuffs, inflammatory molecules and EMMPRIN, and these were abrogated by minocycline. Overall, minocycline attenuated the activation-induced elevation of EMMPRIN on T cells in culture and in EAE mice, correspondent with reduced immune function and EAE CNS pathology.

show abstract

Inhibition of CD147 Gene Expression via RNA Interference Reduces Tumor Cell Proliferation, Activation, Adhesion, and Migration Activity in the Human Jurkat T-Lymphoma Cell Line

Cited by 28 publications

References 35 publications

Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

Basigin Mediates Pulmonary Hypertension by Promoting Inflammation and Vascular Smooth Muscle Cell Proliferation

A novel functional site of extracellular matrix metalloproteinase inducer (EMMPRIN) that limits the migration of human uterine cervical carcinoma cells

Impact of Minocycline on Extracellular Matrix Metalloproteinase Inducer, a Factor Implicated in Multiple Sclerosis Immunopathogenesis

Contact Info

Product

Resources

About