Wip1 knockout inhibits the proliferation and enhances the migration of bone marrow mesenchymal stem cells

Tang, Yiting; Liu, Lan; Sheng, Ming; Xiong, Kai; Huang, Lei; Gao, Qian; Wei, Jingliang; Wu, Tingfang; Yang, Shulin; Liu, Honglin; Mu, Yulian; Li, Kui

doi:10.1016/j.yexcr.2015.03.018

Cited by 20 publications

(15 citation statements)

References 46 publications

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“…Previous studies have shown that Wip1 regulates cellular metastasis in different cell types including neutraphil [ 7 , 8 ], bone marrow mesenchymal stem cell [ 9 ], salivary adenoid cystic carcinoma [ 10 ], while we show here that Wip1 suppresses cellular metastasis in ovarian carcinoma. Despite the oncogenic role of Wip1 was reported in others carcinomas, we revealed an antitumor function of Wip1 in serous ovarian cancer cells.…”

Section: Discussionsupporting

confidence: 64%

“…Zhao et al [ 7 , 8 ] reported that Wip1 might negatively regulate neutrophil migration through regulating p38 MAPK activity. Li et al [ 9 ] found that Wip1 knockout enhanced the migration of bone marrow mesenchymal stem cells. Paradoxically, several other studies suggest that Wip1 may enhance migration or invasion in some carcinomas [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Wip1 suppresses ovarian cancer metastasis through the ATM/AKT/Snail mediated signaling

et al. 2016

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Inactivation of p53 greatly contributes to serous ovarian cancer, while the role of the wild-type p53 induced phosphatase 1 (Wip1) is quite unclear. In this study, by silencing or overexpression of Wip1, we found that Wip1 suppressed ovarian cancer cell invasion, migration, epithelial to mesenchymal transition (EMT), and ovarian cancer metastasis in xenograft animal models. Mechanistic studies showed that Wip1 may block ovarian cancer metastasis through inhibition of Snail and p-Akt expression because silencing or overexpression of Wip1 either upregulated or downregulated the expression of Snail and p-Akt (Ser 473), while further knockdown of Snail by shRNA or inhibition of p-Akt by a chemical compound attenuated cell invasion, migration and EMT in Wip1 silencing cells. We also found that the phosphorylation of Akt at Ser 473 might be mediated through p-ATM (Ser 1981). Thus, Wip1 may suppress ovarian cancer metastasis through negative regulation of p-ATM, p-Akt, and Snail, which was also evidenced in the limited clinical specimens. Therefore, our data may provide a novel therapeutic indication for serous ovarian cancer based on the uncovered mechanism associated with the precise function of Wip1 independent of p53.

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Wip1 suppresses ovarian cancer metastasis through the ATM/AKT/Snail mediated signaling

et al. 2016

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“…The gene encoding human Wip1, PPM1D, is highly expressed in testis (11). Wip1 phosphatase was originally studied as a potent regulator of tumorigenesis (12,13), and emerging evidence has indicated roles for Wip1 in multiple physiological processes and pathophysiological conditions, such as cellular homeostasis (14), neutrophil migration and inflammation (15), B-cell development (16), bone marrow mesenchymal stem cells and macrophage migration (17,18), autophagy, obesity, and atherosclerosis (19). Moreover, Wip1knockout (Wip1-KO) mice presented with defects of the male reproductive organs and impaired spermatogenesis, eventually leading to reduced fertility (11,20).…”

mentioning

confidence: 99%

Integrative Proteomic and Phosphoproteomic Profiling of Testis from Wip1 Phosphatase-Knockout Mice: Insights into Mechanisms of Reduced Fertility**

Wei

Gao

Niu

et al. 2019

Molecular & Cellular Proteomics

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Wei et al. apply multi-layer proteomic profiling and systems biology approaches to define Wip1-deficient testis proteome and phosphoproteome landscapes, and they identify cell adhesion/tight junction, sperm motility, and inflammatory response pathways. These data establish the mechanism that proinflammatory cytokines may impair the blood-testis barrier dynamics by decreasing the expression of junction-associated proteins in Wip1 null testes, leading to subfertility and spermatogenesis defects.

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“…Wip1 −/− mice are more susceptible to infection due to the presence of abnormal lymphoid structure and defective T- and B- cell responses [28]. Meanwhile, Wip1 played an important role in regulation of cell proliferation [29, 30]. Overexpression of Wip1 is observed in human gliomas, and PPM1D silencing suppresses proliferation of human glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Expression of wild-type p53-induced phosphatase 1 in diabetic epiretinal membranes

Zhong

Cui

et al. 2017

Oncotarget

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ObjectiveThe aims of the present study were to investigate the expression and distribution of Wild-type p53-induced phosphatase 1 (Wip1) in diabetic patients with proliferative diabetic retinopathy (PDR) with epiretinal membranes (ERMs) meanwhile analyze the colocalization of Wip1 and nuclear factor kappa-B (NF-κB) p65 in ERMs.MethodsERMs samples were collected from patients with PDR (PDR group) or non-diabetic patients with idiopathic epiretinal membranes (iERMs) (control group) during pars plana vitrectomy. Real-Time PCR analysis was carried out to examine the mRNA expression of Wip1 in ERMs. Immunohistochemical analysis and Immunofluorescent analysis were performed to detect the protein expression of Wip1 in ERMs. Double immunofluorescent staining was performed to detect the colocalization of Wip1 and glial fibrillary acidic protein (GFAP) (retinal glial cells marker), also Wip1 and NF-κB.ResultsERMs were obtained from 17 eyes of 17 patients with PDR (the PDR group) and 9 eyes of 9 nondiabetic patients (the control group) with iERMs. Our results showed high expression levels of Wip1 mRNAs in ERMs after PDR, but low in iERMs. In addition, both immunohistochemistry and immunofluorescence assay showed strong immunoreactivity for Wip1 in PDR ERMs. Furthermore, Wip1 and GFAP were coexpressed in PDR membranes. Finally, the expression of Wip1 was paralleled with NF-κB.ConclusionThese data support the notion that Wip1 contributes to the formation of the ERMs in PDR membranes via NF-κB signaling.

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Wip1 knockout inhibits the proliferation and enhances the migration of bone marrow mesenchymal stem cells

Cited by 20 publications

References 46 publications

Wip1 suppresses ovarian cancer metastasis through the ATM/AKT/Snail mediated signaling

Wip1 suppresses ovarian cancer metastasis through the ATM/AKT/Snail mediated signaling

Integrative Proteomic and Phosphoproteomic Profiling of Testis from Wip1 Phosphatase-Knockout Mice: Insights into Mechanisms of Reduced Fertility**

Expression of wild-type p53-induced phosphatase 1 in diabetic epiretinal membranes

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