Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

Jia, Shuqin; Qu, Tingting; Feng, Mengmeng; Ji, Ke; Li, Ziyu; Jiang, Wen Guo; Ji, Jiafu

doi:10.1177/1010428317699755

Cited by 23 publications

(17 citation statements)

References 25 publications

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“…Based on the involvement of CCN4 in many other cancers, Jia et al tested whether there was an association of CCN4 with gastric cancer 29. This group determined that CCN4 mRNA levels were elevated in gastric cancer specimens, and that CCN4 was expressed in gastric carcinoma cell lines.…”

Section: Gastric Cancermentioning

confidence: 99%

The role of CCN4/WISP-1 in the cancerous phenotype

Nivison¹,

Meier²

2018

CMAR

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CCN proteins are secreted into the extracellular environment where they interact with both components of the extracellular matrix and with cell surface receptors to regulate cellular function. Through these interactions, CCNs act as extracellular ligands to activate intracellular signal transduction pathways. CCN4/WISP-1, like other CCNs, plays multiple physiologic roles in development and also participates in pathogenesis. CCN4 is of particular interest with respect to cancer, showing promise as a biomarker or prognostic factor as well as a potential therapeutic target. This review focuses on recent work addressing the role of CCN4 in cancer. While CCN4 has been identified as an oncogene in a number of cancers, where it enhances cell migration and promoting epithelial–mesenchymal transition, there are other cancers where CCN4 appears to play an inhibitory role. The mechanisms underlying these differences in cellular response have not yet been delineated, but are an active area of investigation. The expression and activities of CCN4 splice variants are likewise an emerging area for study. CCN4 acts as an autocrine factor that regulates the cancer cells from which it is secreted. However, CCN4 is also a paracrine factor that is secreted by stromal fibroblasts, and can affect the function of vascular endothelial cells. In summary, current evidence is abundant in regard to establishing potential roles for CCN4 in oncogenesis, but much remains to be learned about the functions of this fascinating protein as both an autocrine and paracrine regulator in the tumor microenvironment.

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Section: Gastric Cancermentioning

confidence: 99%

The role of CCN4/WISP-1 in the cancerous phenotype

Nivison¹,

Meier²

2018

CMAR

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“…Notably, the CCN (Cyr61, CTGF, and NOV) membrane proteins are essential in tumorigenesis and metastasis 15 . The CNN family also plays regulatory roles in angiogenesis and tumorigenesis 16 . Our previous work indicates that CCN6 regulates metastasis in chondrosarcoma, enhancing chondrosarcoma cell migration by increasing levels of ICAM-1 expression 17 .…”

Section: Introductionmentioning

confidence: 99%

CCN6-mediated MMP-9 activation enhances metastatic potential of human chondrosarcoma

Tzeng

Tang

et al. 2018

Cell Death Dis

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Chondrosarcomas are primary malignant bone tumors that have a poor prognosis. WNT1-inducible signaling pathway protein-3 (WISP-3, also termed CCN6) belongs to the CCN family of proteins and is implicated in the regulation of various cellular functions, such as cell proliferation, differentiation, and migration. It is unknown as to whether CCN6 affects human chondrosarcoma metastasis. We show how CCN6 promotes chondrosarcoma cell migration and invasion via matrix metallopeptidase-9 (MMP)-9 expression. These effects were abolished by pretreatment of chondrosarcoma cells with PI3K, Akt, mTOR, and NF-κB inhibitors or short interfering (si)RNAs. Our investigations indicate that CCN6 facilitates metastasis through the PI3K/Akt/mTOR/NF-κB signaling pathway. CCN6 and MMP-9 expression was markedly increased in the highly migratory JJ012(S10) cell line compared with the primordial cell line (JJ012) in both in vitro and in vivo experiments. CCN6 knockdown suppressed MMP-9 production in JJ012(S10) cells and attenuated cell migration and invasion ability. Importantly, CCN6 knockdown profoundly inhibited chondrosarcoma cell metastasis to lung. Our findings reveal an important mechanism underlying CCN6-induced metastasis and they highlight the clinical significance between CCN6 and MMP-9 in regard to human chondrosarcoma. CCN6 appears to be a promising therapeutic target in chondrosarcoma metastasis.

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“…Our previous study has also demonstrated that Tp53 mutation may promote WISP1 expression in mouse PDAC cells ( Wang et al, 2015 ). Recent studies had shown that WISP1 acts as a new oncogene in glioblastoma ( Jing et al, 2017 ), oral squamous cell carcinoma ( Jung et al, 2017 ), gastric cancer ( Jia et al, 2017 ), melanoma ( Shao et al, 2016 ), and colon cancer ( Wu et al, 2016 ). Also, Yang et al (2015) showed that patients with high expression of WISP-1 had a shorter survival time independent of clinical stage and lymphatic metastasis status in pancreatic cancer.…”

Section: Discussionmentioning

confidence: 99%

Tp53 Mutation Inhibits Ubiquitination and Degradation of WISP1 via Down-Regulation of Siah1 in Pancreatic Carcinogenesis

Liu

Wei

et al. 2018

Front. Pharmacol.

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Wnt1 inducible signaling pathway protein-1 (WISP1) may play an important role in promoting carcinogenesis. However, the biological function and underlying mechanism of WISP1 in pancreatic carcinogenesis still remains enigmatic. In this study, immunochemistry staining showed that protein levels of WISP1 were more significantly upregulated in pancreatic ductal adenocarcinoma (PDAC) tissues with Tp53 mutation than in PDAC tissues with Tp53 wild-type. In addition, a significant correlation was observed between increased malignant phenotype of tumors from well-differentiated adenocarcinoma tissues to moderately- or poorly-differentiated adenocarcinoma tissues shifting from cytoplasmic expression to nuclear accumulation of WISP1. Interestingly, WISP1 expression was correlated with the poor prognosis in PDAC patients with Tp53 mutation. Also, the biological function analysis showed that WISP1 may act as a potential oncogene in PDAC cells. In addition, immunofluorescence analysis showed that Tp53 mutation promoted WISP1 expression in PanIN and PDAC cells, while Siah E3 Ubiquitin Protein Ligase 1 (Siah1) inhibited WISP1 expression in PDAC cells. Moreover, through immunoprecipitation, immunoblotting analysis, in vitro binding assay, and ubiquitination assay, we found that Tp53 mutation inhibited ubiquitination and degradation of Siah1-dependent WISP1. Therefore, Tp53 mutation-Siah1-WISP1 is a new signaling pathway, playing an important role in pancreatic carcinogenesis.

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Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

Cited by 23 publications

References 25 publications

The role of CCN4/WISP-1 in the cancerous phenotype

The role of CCN4/WISP-1 in the cancerous phenotype

CCN6-mediated MMP-9 activation enhances metastatic potential of human chondrosarcoma

Tp53 Mutation Inhibits Ubiquitination and Degradation of WISP1 via Down-Regulation of Siah1 in Pancreatic Carcinogenesis

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