Motility-related protein (MRP-1/CD9) and KAI1/CD82 expression inversely correlate with lymph node metastasis in oesophageal squamous cell carcinoma

Uchida, Satoshi; Shimada, Yutaka; Watanabe, Go; Li, Z Gang; Hong, Tao; Miyake, Masayuki; Imamura, Masayuki

doi:10.1038/sj.bjc.6690186

Cited by 93 publications

(74 citation statements)

References 12 publications

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“…Moreover, we revealed that reduced MRP-1/CD9 expression was associated with a poor prognosis in patients with breast cancers, non-small cell lung cancers (NSCLC) and pancreatic cancers (Miyake et al, 1996;Higashiyama et al, 1995;Sho et al, 1998). In addition, other laboratories reported the same phenomenon in colon cancer and esophageal cancer (Mori et al, 1998;Uchida et al, 1999). Thus, this gene suppresses tumor metastasis in various cancers, and its decreased expression may be involved in malignant progression.…”

Section: Introductionsupporting

confidence: 53%

Suppression of pulmonary metastasis using adenovirally motility related protein-1 (MRP-1/CD9) gene delivery

et al. 2000

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Previously we showed that MRP-1/CD9 might prevent tumor metastasis by suppression of cell motility and invasion of tissue barriers. The present study explored the possibility of preventing metastasis of mouse melanoma BL6 by expression of MRP-1/CD9 through gene transfer. A replication-de®cient adenovirus vector was used for the in vivo transfer of MRP-1/CD9 cDNA. Intratumor injection of an adenovirus vector (rAd-MRP-1/CD9) expressing MRP-1/CD9 resulted in a 73.7% reduction in the number of pulmonary metastases of mice and the median survival time of mice treated with rAd-MRP-1/CD9 was signi®cantly longer than those treated with the rAd-b-gal vector (103.2+8.5 days vs 71.2+5.2 days, P50.001 respectively). These results support the expression of MRP-1/CD9 through gene transfer as a therapeutic strategy for preventing metastases and prolonging survival, and support the feasibility of gene transfer in a clinically relevant setting. Oncogene (2000) 19, 5221 ± 5226.

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Section: Introductionsupporting

confidence: 53%

Suppression of pulmonary metastasis using adenovirally motility related protein-1 (MRP-1/CD9) gene delivery

et al. 2000

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“…5,7,10,34 The involvement of the CD9 molecule in metastasis has been further inferred from the inhibition of tumor cell motility and migration caused by CD9 specific mAbs or by overexpression of this tetraspanin. 5,7,9,10 While this implication of CD9 in metastasis has been documented in numerous studies and is fairly well established, much less attention has been however devoted to the possi- ble involvement of this tetraspanin in the early stages of tumor formation, i.e.…”

Section: Discussionmentioning

confidence: 99%

The tetraspanin CD9 inhibits the proliferation and tumorigenicity of human colon carcinoma cells

Ovalle

Gutiérrez-López

Olmo

et al. 2007

Intl Journal of Cancer

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The implication of the tetraspanin CD9 in cancer has received much recent attention and an inverse correlation between CD9 expression and the metastatic potential and cancer survival rate has been established for different tumor types. In contrast to the well-established role of CD9 in metastasis, very little is known about the involvement of this tetraspanin in the process of development of primary tumors. In the present study, we present evidence on the implication of CD9 in colon carcinoma tumorigenesis. We report here that ectopic expression of CD9 in colon carcinoma cells results in enhanced integrin-dependent adhesion and inhibition of cell growth. Consistently with these effects, treatment of these cells with anti-CD9-specific antibodies resulted in (i) increased b1 integrin-mediated cell adhesion through a mechanism involving clustering of integrin molecules rather than altered affinity; (ii) induction of morphological changes characterized by the acquisition of an elongated cell phenotype; (iii) inhibition of cell proliferation with no significant effect on cell survival; (iv) increased expression of membrane TNF-a, and finally (v) inhibition of the in vivo tumorigenic capacity in nude mice. In addition, through the use of selective blockers of TNF-a, we have demonstrated that this cytokine partly mediates the antiproliferative effects of CD9. These results clearly establish for the first time a role for CD9 in the tumorigenic process. ' 2007 Wiley-Liss, Inc.Key words: CD9; TNF-a; proliferation; tumorigenicity; tetraspanin The tetraspanin CD9 is a widely distributed surface molecule implicated in diverse functions, including cell signaling, growth, adhesion and motility, metastasis and sperm-egg fusion. Like other members of the tetraspanin protein family, CD9 participates in the organization of cell surface protein microdomains, termed ''the tetraspanin web,'' through association with other transmembrane proteins including members of the integrin family of adhesion receptors. [1][2][3] The implication of CD9 in cancer has received much attention. An inverse correlation between its expression in primary tumors and the metastatic potential and patient survival rate has been established for melanomas and colon, lung and breast carcinomas. 1,4-8 The involvement of this tetraspanin in tumor progression has been inferred from the effects of CD9 antibodies or CD9 overexpression on tumor cell motility and migration. In this regard, it has been shown that overexpression of this tetraspanin in melanoma and breast, lung, pancreas and colon carcinoma cells suppresses the motility and metastatic potential of these cells. 5,7,9,10 mAbs directed to the CD9 molecule have also been shown to inhibit the migration of different types of carcinoma tumor cells and the transendothelial migration of melanoma cells. 11-13 Therefore, the inverse correlation observed between CD9 expression and the metastatic potential could be explained, at least in part, by the effects mediated by CD9 on cell adhesion and migration through the ...

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“…In order to define the location of the plasma membrane more clearly, the cells were treated with an antibody against the CD-9 protein, that is located on the plasma membrane in a number of cell types. 24,33 Immunofluorescence images of LNCaP cells treated with the anti-CD-9 antibody revealed a clear location of the CD-9 protein at the plasma membrane of cells transfected with pCMV-EGFP-TRPL (Fig 3b) and cells transfected with pCMV-EGFP-C1 (Fig 3e). Overlay of the CD-9 and EGFP-TRPL images for each cell transfected with pCMV-EGFP-TRPL showed that the EGFP-TRPL chimeric protein and the CD-9 protein are colocated at the plasma membrane in a band (about 30-50% of the plasma membrane) of the cell (Fig 3c, indicated by the orange color (arrows)).…”

Section: Expression Of the Trpl Protein In Transiently Transfected Lnmentioning

confidence: 99%

Expression of Drosophila Ca2+ permeable transient receptor potential-like channel protein in a prostate cancer cell line decreases cell survival

et al. 2003

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The effects of expression of Drosophila melanoga ster Ca 2+ permeable transient receptor potential-like (TRPL) channels, under the control of the cytomegalovirus (CMV) or prostate cell-specific promoters, on cell survival and apoptosis in the androgen-sensitive LNCaP prostate cancer cell line were investigated. A prostate-specific antigen (PSA) promoter construct (designated PSAEn/PSAPr) composed of a 0.6 kb region of the promoter and a 1.45 kb region of the enhancer resulted in androgen-dependent and prostatespecific expression of a luciferase reporter gene in transiently transfected LNCaP cells. Expression of the enhanced green fluorescence protein-TRPL chimeric protein under the control of the CMV promoter was confirmed by Western blot. Whereas the majority of the expressed protein was located in the cytoplasmic space, confocal microscopy with the CD-9 protein as a plasma membrane marker demonstrated that approximately 10% of the expressed TRPL protein was located in a band in the plasma membrane. Using recombinant adenoviruses, expression of the TRPL protein was associated with an increase in both the initial and sustained rates of Ca 2+ inflow. Expression of TRPL under the control of the CMV promoter for 96 hours decreased cell number and increased the number of cells undergoing apoptosis by 23 and 27%, respectively. Apoptosis was inhibited by a caspase-3 inhibitor, Z-DEVD-fmk. It is concluded that, when heterologously expressed in LNCaP cells, the TRPL protein leads to a reduction in cell survival due, in part, to the induction of apoptosis. The effects of TRPL are likely caused by enhanced Na + and Ca 2+ inflow to the cells. This finding suggests a novel approach to modify the growth of prostate cancer cells that fail to undergo apoptosis following androgen ablation therapy.

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Motility-related protein (MRP-1/CD9) and KAI1/CD82 expression inversely correlate with lymph node metastasis in oesophageal squamous cell carcinoma

Cited by 93 publications

References 12 publications

Suppression of pulmonary metastasis using adenovirally motility related protein-1 (MRP-1/CD9) gene delivery

Suppression of pulmonary metastasis using adenovirally motility related protein-1 (MRP-1/CD9) gene delivery

The tetraspanin CD9 inhibits the proliferation and tumorigenicity of human colon carcinoma cells

Expression of Drosophila Ca2+ permeable transient receptor potential-like channel protein in a prostate cancer cell line decreases cell survival

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