Levels of expression of pleiotrophin and protein tyrosine phosphataseζ are decreased in human colorectal cancers

Yamakawa, Taishi; Kurosawa, Nobuyuki; Kadomatsu, Kenji; Matsui, Takanori; Itoh, Kosuke; Maeda, Nobuaki; Noda, Masaharu; Muramatsu, Takashi

doi:10.1016/s0304-3835(98)00275-4

Cited by 25 publications

(18 citation statements)

References 20 publications

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“…In gliomastoma the expression of RPTP␤/ is increased compared with normal brain tissues (8) and in human astrocytic tumor cells, the up-regulated expression of RPTP␤/ and pleiotrophin creates an autocrine loop that is important for cell migration (9). However, pleiotrophin and RPTP␤/ expression were found decreased in human colorectal cancers (51).…”

Section: Discussionmentioning

confidence: 99%

Loss of Receptor Protein Tyrosine Phosphatase β/ζ (RPTPβ/ζ) Promotes Prostate Cancer Metastasis

Diamantopoulou

Kitsou

Ménashi

et al. 2012

Journal of Biological Chemistry

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Background:The role of pleiotrophin and its receptors RPTP␤/ and Syndecan-3 during tumor metastasis remains unknown. Results: RPTP␤/ knockdown initiates EMT, promotes pleiotrophin-mediated migration and attachment through Syndecan-3 and induces in vivo metastasis. Conclusion: RPTP␤/ plays a suppressor-like role in prostate cancer metastasis. Significance: Boosting RPTP␤/ or attenuating Syndecan-3 signaling pathways may lead to more effective therapeutic strategies in treating prostate cancer metastasis.

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Section: Discussionmentioning

confidence: 99%

Loss of Receptor Protein Tyrosine Phosphatase β/ζ (RPTPβ/ζ) Promotes Prostate Cancer Metastasis

Diamantopoulou

Kitsou

Ménashi

et al. 2012

Journal of Biological Chemistry

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“…For example, PTN acts as an angiostatic factor in an in vivo neuroblastoma model resistant to the DNA-topoisomerase I inhibitor irinotecan, 32 and NO has been also reported as an antiangiogenic molecule in neuroblastomas. 33 The mRNA levels of both PTN and RPTPb/f are decreased in colorectal cancers as compared with those in adjacent normal mucosa 34 and eNOS expression in colorectal carcinoma is significantly lower than in non-neoplasm colorectal mucosa, 35 while NO induces apoptosis in colon cancer cells 36,37 via ERK[1/2] activation. 37 PTN is increased in non-tumor-bearing skin adjacent to excised squamous cell carcinomas 38 and eNOS-transfected oral carcinoma SCC-25 cells have decreased growth rate in vitro and in vivo compared with the wild-type parental or vector control-transfected cells.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide stimulates migration of human endothelial and prostate cancer cells through up‐regulation of pleiotrophin expression and its receptor protein tyrosine phosphatase β/ζ

Polytarchou

Hatziapostolou

Poimenidi

et al. 2009

Intl Journal of Cancer

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Pleiotrophin (PTN) is a secreted growth factor involved in angiogenesis and tumor growth. We have recently shown that low concentrations of hydrogen peroxide (HP) stimulate PTN expression, through activation of the transcription factor AP-1. In the present work, we studied the possible involvement of endothelial nitric oxide synthase (eNOS) and the role of nitric oxide (NO) in the regulation of PTN expression, as well as involvement of the latter in the NO-induced human endothelial and prostate cancer cell migration. Inhibition of eNOS or the downstream effector soluble guanylate cyclase (sGC) completely suppressed HP-induced AP-1 activities that lead to PTN expression and cell migration. The NO donor sodium nitroprusside (SNP) through activation of sGC significantly and concentration-dependently increased expression of PTN, through transcriptional activation of the corresponding gene. Moreover, SNP had no effect on the migration of stably transfected prostate cancer cells that do not express PTN and knockdown of PTN receptor protein tyrosine phosphatase b/f (RPTPb/f) completely abolished SNP-induced cell migration. NO added exogenously or produced endogenously by low concentrations of HP through stimulation of sGC activates extracellular signal-regulated kinase[1/2] (ERK[1/2]) and leads to PTN expression and cell migration. On the other hand, p38, which also intervenes in the up-regulation of PTN expression by low concentrations of HP, seems to act upstream of eNOS and does not intervene in the SNP-induced PTN expression and cell migration. The above data suggest that PTN through its receptor RPTPb/f is a mediator of the stimulatory effects of eNOS/NO on human endothelial and prostate cancer cell migration. '

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“…The same holds true for the signaling molecule HEK2 [12] (Table 1). HBNF-1 (also known as pleiotrophin, Table 3) and protein tyrosine phosphatase zeta (Table 1), decreased in colorectal tumors compared with normal tissue [38], are downregulated by radiation only in normal tissue.…”

Section: Discussionmentioning

confidence: 99%

Radiation induces different changes in expression profiles of normal rectal tissue compared with rectal carcinoma

et al. 2004

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Levels of expression of pleiotrophin and protein tyrosine phosphataseζ are decreased in human colorectal cancers

Cited by 25 publications

References 20 publications

Loss of Receptor Protein Tyrosine Phosphatase β/ζ (RPTPβ/ζ) Promotes Prostate Cancer Metastasis

Loss of Receptor Protein Tyrosine Phosphatase β/ζ (RPTPβ/ζ) Promotes Prostate Cancer Metastasis

Nitric oxide stimulates migration of human endothelial and prostate cancer cells through up‐regulation of pleiotrophin expression and its receptor protein tyrosine phosphatase β/ζ

Radiation induces different changes in expression profiles of normal rectal tissue compared with rectal carcinoma

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