Disease relevance of WISP1

• In summary, these results suggest that CTGF, WISP-1, and CYR61 may play a role in the progression of breast cancer and might serve as a valuable tool for monitoring tumor status of breast cancer patients [1].
• Overexpression of WISP-1 down-regulated motility and invasion of lung cancer cells through inhibition of Rac activation [2].
• We demonstrated that overexpression of WISP-1 in H460 lung cancer cells inhibited lung metastasis and in vitro cell invasion and motility [2].
• WNT1 inducible signaling pathway protein 3, WISP-3, a novel target gene in colorectal carcinomas with microsatellite instability [3].
• OBJECTIVE: To determine whether Wnt-1-inducible signaling pathway protein 3 (WISP3) polymorphisms are associated with susceptibility to juvenile idiopathic arthritis (JIA) [4].

High impact information on WISP1

• WISP-1 acts to block cell death at a late stage in the p53-mediated apoptosis pathway [5].
• Here it is shown that WISP-1 can activate the antiapoptotic Akt/PKB signaling pathway [5].
• It also is demonstrated that WISP-1 can prevent cells from undergoing apoptosis following DNA damage through inhibition of the mitochondrial release of cytochrome c and up-regulation of antiapoptotic Bcl-X(L) [5].
• WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase [5].
• WISP-1 (Wnt-1-induced secreted protein) was identified as an oncogene regulated by the Wnt-1-beta-catenin pathway [5].

Chemical compound and disease context of WISP1

• Effect of indomethacin on Bfl-1, WISP-1 and proliferating cell nuclear antigen in colon cancer cell line HCT116 cells [6].

Biological context of WISP1

• Moreover, we identified two novel variants, generated by alternative splicing of WISP1 and WISP3, respectively, named WISP1 delta ex3-4 and WISP3vL [7].
• WISP-1 demonstrated oncogenic activities; overexpression of WISP-1 in normal rat kidney fibroblast cells (NRK-49F) induced morphological transformation, accelerated cell growth, and enhanced saturation density [8].
• This work illustrates a negatively regulated pathway by WISP-1 involving integrins and Rac in the down-regulation of invasion [2].
• In our previous study, COX-2 independent proteins (Bfl-1, WISP-1 and proliferating cell nuclear antigens [PCNA]) in indomethacin-treated colorectal cancer cells with the use of proteomics technology had been identified [6].

Anatomical context of WISP1

• Our results show for the first time that WISP1, WISP1v, and WISP3 are expressed in HCC cell lines [7].
• To monitor the expression of CCN4/WISP1 mRNA along chondrocyte differentiation, RGC cells were cultured and sampled until they were mineralized [9].
• WISP-1 mRNA expression was identified in normal and transformed cell lines [10].

Associations of WISP1 with chemical compounds

• Indomethacin also down-regulated the expression of Bfl-1, WISP-1 and PCNA protein (40.01 +/- 1.61 vs 43.76 +/- 1.63, 22.50 +/- 1.17 vs 30.30 +/- 1.55, 17.69 +/- 1.18 vs 20.80 +/- 1.08) [6].

Other interactions of WISP1

• CONCLUSIONS: Early induction of WNT5A, coupled with the coordinated induction and repression of genes that modulate the Wnt signaling pathway, led to the early, selective induction of WISP1 and no other Wnt-inducible genes [11].
• Differential expression of WISP-1 and WISP-2 genes in normal and transformed human breast cell lines [10].
• In an invasion assay across collagen I, an MMP-1 target matrix, WISP-1 cells were significantly less invasive compared with controls, whereas WISP-1/RacG12V cells showed elevated invasion levels [2].
• We found a strong correlation between WISP-1 and COL11A1 expression in sporadic carcinomas [12].
• Increased expression of cyclin D1, c-myc, and WISP-1 mRNAs in HMEG suggested activation of the Wnt-1/beta-catenin cascade [13].

Analytical, diagnostic and therapeutic context of WISP1

• We performed microarray and real-time PCR analyses to identify genes involved in invasion that may be differentially regulated by WISP-1 [2].
• Using differential display, RT-PCR and DNA sequencing analyses in normal human mammary epithelial cells (HMEC) and various breast tumor cell lines including MCF-7, ZR-75, T-47D and SKBR2, we demonstrated that WISP-1 and WISP-2 genes are differentially transcribed in these cells [10].
• The expression of Bfl-1, WISP-1 and PCNA, mRNA and protein were determined by a real-time quantitative PCR and Western blot, respectively [6].

References