Expression of METH-1 and METH-2 in pancreatic cancer

Masui, Toshihiko; Hosotani, Ryo; Tsuji, S.; Miyamoto, Yoshiharu; Yasuda, Sachiyo; Ida, Jun; Nakajima, Saeko; Kawaguchi, Michiya; Kobayashi, Hiroyuki; Koizumi, Masayuki; Toyoda, Eiji; Tulachan, Sidhartha; Arii, Shigeki; Doi, Ryuichiro; Imamura, Masayuki

doi:10.1016/s0016-5085(01)81290-7

Cited by 43 publications

(28 citation statements)

References 29 publications

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“…In the present study ADAMTS1 was significantly down-regulated in prostate cancer compared to benign prostate tissue, which indicates that ADAMTS1 is involved in the regulation of tumour progression. This result is in accordance with previous studies showing lower levels of ADAMTS1 in human breast, pancreatic, hepatocellular and lung cancer than in non-neoplastic tissue [19][20][21]. To our knowledge the present study is the first describing the expression of ADAMTS1 in human prostate cancer.…”

Section: Discussionsupporting

confidence: 94%

“…In the HN tumours there was no difference in MVD between tumours expressing low or moderate/high levels of ADAMTS1. This was also the situation in pancreatic and hepatocellular cancer, where no correlation was found between ADAMTS1 and MVD [20].…”

Section: Fig 2 Expression Of Adamts1 Was Analysed By Immunohistochementioning

confidence: 67%

“…However, it has also been reported that ADAMTS1 can function as a pro-angiogenic and pro-tumorigenic factor, depending on the activity and proteolytic status of the protein [8,17,18]. In clinical cancer, the role of ADAMTS1 has not been extensively 1 7 8 7 investigated, but lower expression levels have been reported in breast, pancreatic, hepatocellular and lung cancer than in benign tissue [19][20][21]. However, in human prostate cancer ADAMTS1 is mostly unexplored.…”

Section: Introductionmentioning

confidence: 99%

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ADAMTS1, a putative anti‐angiogenic factor, is decreased in human prostate cancer

Gustavsson¹,

Wang²,

Jennbacken³

et al. 2009

BJU International

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quantified by counting the number of CD34-positive blood vessels. RESULTSADAMTS1 was strongly expressed in the luminal epithelial cells in benign prostate glands, whereas expression was significantly lower in prostate cancer cells. There was no obvious difference between hormone-naïve and hormone-refractory tumours, and ADAMTS1 expression did not correlate with Gleason score. However, in hormonerefractory tumours from patients with metastatic disease, the expression of ADAMTS1 was significantly lower than in tumours from patients without metastases. Furthermore, the MVD was higher in hormone-refractory than in hormone-naïve tumours and benign tissue, and MVD correlated with Gleason score. There was no association between ADAMTS1 and MVD in the hormone-naïve tumours, while hormone-refractory tumours with low ADAMTS1 expression had a higher MVD than those with moderate/high expression. CONCLUSIONADAMTS1 expression is decreased in prostate cancer, and might be involved in the early steps of prostate cancer development. Further, ADAMTS1 might have an antiangiogenic and antimetastatic role in hormone-refractory prostate cancer, where low ADAMTS1 expression is associated with a high MVD and metastasis. KEYWORDSADAMST1, angiogenesis, androgen independent, microvessel density, prostate cancer OBJECTIVETo investigate the expression of 'ADAM metallopeptidase with thrombospondin type

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Section: Discussionsupporting

confidence: 94%

Section: Fig 2 Expression Of Adamts1 Was Analysed By Immunohistochementioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

ADAMTS1, a putative anti‐angiogenic factor, is decreased in human prostate cancer

Gustavsson¹,

Wang²,

Jennbacken³

et al. 2009

BJU International

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“…Genes that were expressed differentially, both in comparison 1 and comparison 2 (''ort intact'' vs. ''sc intact'' and ''ort intact'' vs. ''ort castrated'') are considered to be the most plausible candidates for causing the repressed growth of LNCaP-19 tumors in the prostate. In the slow-growing orthotopic tumors (''ort intact''), we found elevated expression of anti-angiogenic and tumor-inhibiting factors, including ADAMTS1 [25][26][27], PCDH20 [28] and RGS2 [29]. Interestingly, RGS2 is involved in inhibition of androgen-independent activation of the androgen receptor.…”

Section: Discussionmentioning

confidence: 94%

The prostatic environment suppresses growth of androgen‐independent prostate cancer xenografts: An effect influenced by testosterone

et al. 2009

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“…We have recently found that AHR drove the reported gene in cancer cells even in the normoxia (data not shown). ADAMTS1 has been reported to respond to a variety of cytokine signals in various cells (Krampert et al, 2005;Kalinski et al, 2007;Choi et al, 2008), and the high expression level of ADAMTS1 in cancer cells was reported (Masui et al, 2001;Stokes et al, 2010). Thus, further careful investigation is needed for the specificity.…”

Section: Discussionmentioning

confidence: 99%

AHR, a novel acute hypoxia-response sequence, drives reporter gene expression under hypoxiain vitroandin vivo

et al. 2010

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ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motifs 1) is an early immediate gene. We have previously reported that ADAMTS1 was strongly induced by hypoxia. In this study, we investigated whether ADAMTS1 promoter-driven reporter signal is detectable by acute hypoxia. We constructed the GFP (green fluorescent protein) expression vector [AHR (acute hypoxia-response sequence)-GFP] under the control of ADAMTS1 promoter and compared it with the constitutive GFP-expressing vector under the control of CMV (cytomegalovirus promoter-GFP). We transduced AHR-GFP and examined whether GFP signals can be detected under the acute hypoxia. When the human umbilical vein [HUVEC (human umbilical vein endothelial cells)] was transduced under normoxia, there were few GFP signals, while CMV-GFP showed considerable GFP signals. When HUVEC was stimulated with hypoxia, GFP signals from AHR-GFP gene were induced under hypoxic conditions. Notably, the GFP signals peaked at 3 h under hypoxia. In ischaemic hind limb model, transduced AHR-GFP showed hypoxic induction of GFP signals. In summary, we have demonstrated that the AHR system induced the reporter gene expression by acute hypoxia, and its induction is transient. This is the first report showing the unique acute hypoxia-activated gene expression system.

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Expression of METH-1 and METH-2 in pancreatic cancer

Cited by 43 publications

References 29 publications

ADAMTS1, a putative anti‐angiogenic factor, is decreased in human prostate cancer

ADAMTS1, a putative anti‐angiogenic factor, is decreased in human prostate cancer

The prostatic environment suppresses growth of androgen‐independent prostate cancer xenografts: An effect influenced by testosterone

AHR, a novel acute hypoxia-response sequence, drives reporter gene expression under hypoxiain vitroandin vivo

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