A novel variant of WISP1 lacking a Von Willebrand type C module overexpressed in scirrhous gastric carcinoma

Tanaka, Shinji; Saeki, Hiroshi; Kinoshita, Jin H.; Ohga, Takefumi; Shimada, Mitsuo; Maehara, Yoshihiko; Sugimachi, Keizō

doi:10.1038/sj.onc.1204723

Cited by 72 publications

(95 citation statements)

References 27 publications

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“…Indeed, it was reported that a naturally occurring variant of WISP-1 called WISP-1v lacks domain-II, which bears significant homology to von Willebrand factor CII and contains a putative transforming growth factor-b/BMPbinding site. WISP1v transfectants enhanced the invasive phenotype of co-cultured gastric carcinoma cells, whereas wild-type WISP1 had no such potential (Tanaka et al, 2001). Moreover, as melanoma is a notoriously heterogeneous tumor, the sensitivity of individual melanoma cell to WISP-1 may not be identical as not all melanoma cells we tested respond to ghWISP-1 treatment.…”

Section: Discussionmentioning

confidence: 95%

Activation of Notch1 signaling in stromal fibroblasts inhibits melanoma growth by upregulating WISP-1

et al. 2011

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Section: Discussionmentioning

confidence: 95%

Activation of Notch1 signaling in stromal fibroblasts inhibits melanoma growth by upregulating WISP-1

et al. 2011

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“…WNT1-inducible signaling pathway protein 1 (WISP1) is induced by WNT1 and belongs to the CCN family, which includes CTGF (connective tissue growth factor), Cyr61 (cysteine-rich 61) and Nov (nephroblastoma-overexpressed gene). 34 WISP1 is a target of the Wnt-b-catenin pathway, with its expression being regulated by b-catenin. 35,36 WISP1 activity and availability are modulated by its interaction with decorin and biglycan, two extracellular matrixassociated proteoglycans that are abundant in bone and cartilage.…”

Section: Discussionmentioning

confidence: 99%

Association of polymorphisms of SORBS1, GCK and WISP1 with hypertension in community-dwelling Japanese individuals

Yamada

Ando

Shimokata³

2009

Hypertens Res

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Although various loci and genes have been implicated in predisposition to hypertension by genetic linkage analyses and candidate gene association studies, the genes that confer susceptibility to this condition remain to be identified definitively. We have now examined the relationships of 22 candidate gene polymorphisms with the prevalence of hypertension and with blood pressure (BP) in a 6-year population-based longitudinal cohort study and observed significant relationships of three polymorphisms of SORBS1, GCK and WISP1 with hypertension. The 2233 subjects (1106 women, 1127 men) were aged 40-79 years and were randomly recruited to a population-based prospective cohort study of aging and age-related diseases in Japan. BP was measured with subjects having rested in the sitting position for at least 15 min. Genotypes for the 682A-G (Thr228Ala) polymorphism of SORBS1, the À30G-A polymorphism of GCK and the 2364A-G polymorphism of WISP1 were determined by melting curve analysis. Longitudinal analysis with a generalized estimating equation revealed that the polymorphisms of SORBS1 and GCK and that of WISP1 were significantly associated with the prevalence of hypertension in women and men, respectively. Longitudinal analysis with a mixed-effect model revealed that the polymorphism of SORBS1 was significantly related to diastolic BP in women and that those of GCK and WISP1 were significantly related to both systolic and diastolic BP in women and men, respectively. These results suggest that SORBS1 and GCK are susceptibility loci for hypertension in Japanese women and that WISP1 is such a locus in men.

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“…In hepatocellular carcinoma, CCN4 (WISP1) is alternatively spliced to produce transcripts encoding (i) CCN4 protein missing the VWC domain and (ii) truncated CCN4 containing only the IGFBP domain (Cervello, Giannitrapani et al 2004). The former is also encoded by spliceforms expressed in gastric carcinoma (Tanaka, Sugimachi et al 2001), thus this cancer-associated spliceform may play an important role in the pathophysiology of these cancers. In breast cancer, alternative splicing and expression of CCN1 is controlled by hypoxia (Hirschfeld, zur Hausen et al 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Alternative splicing of other CCN family mRNAs including CCN1, CCN3 and CCN4 has been reported in the last decade (Perbal 2009). Furthermore WNT1/CCN4 transcript variants have been observed in gastric carcinoma, and hepatoma (Tanaka, Sugimachi et al 2001;Cervello, Giannitrapani et al 2004), while alternative CYR61 (CCN1) transcripts have been identified in breast cancer cell lines (Hirschfeld, zur Hausen et al 2009). …”

Section: Introductionmentioning

confidence: 99%

Novel CT domain-encoding splice forms of CTGF/CCN2 are expressed in B-lineage acute lymphoblastic leukaemia

et al. 2015

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A novel variant of WISP1 lacking a Von Willebrand type C module overexpressed in scirrhous gastric carcinoma

Cited by 72 publications

References 27 publications

Activation of Notch1 signaling in stromal fibroblasts inhibits melanoma growth by upregulating WISP-1

Activation of Notch1 signaling in stromal fibroblasts inhibits melanoma growth by upregulating WISP-1

Association of polymorphisms of SORBS1, GCK and WISP1 with hypertension in community-dwelling Japanese individuals

Novel CT domain-encoding splice forms of CTGF/CCN2 are expressed in B-lineage acute lymphoblastic leukaemia

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