Dual effect of WISP-1 in diverse pathological processes

Feng, Mengmeng; Jia, Shuqin

doi:10.21147/j.issn.1000-9604.2016.06.01

Cited by 14 publications

(12 citation statements)

References 48 publications

(46 reference statements)

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“…Like other CCNs, CCN4 contains four conserved cysteine-rich domains that interact with other proteins. 2 , 3 Within the CCN family, CCN4 is most similar to CCN3/WISP-3. 3 CCN proteins are characterized by four highly conserved domains ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

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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: Introductionmentioning

confidence: 99%

“… 2 , 3 Within the CCN family, CCN4 is most similar to CCN3/WISP-3. 3 CCN proteins are characterized by four highly conserved domains ( Figure 1 ). The differentiating, nonconserved region is a protease-sensitive “hinge” located after exon 3, the von Willebrand factor type C domain.…”

Section: Introductionmentioning

confidence: 99%

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

Nivison¹,

Meier²

2018

CMAR

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“…30 WISP1 is widely expressed in a variety of human organs and plays an important role in many pathophysiological processes, including embryonic development, inflammation, injury repairs, and tumor progression. 31 In recent years, studies have found that WISP1 is abnormally expressed in a variety of cancers and promotes tumor growth, metastasis, and epithelial-to-mesenchymal transition (EMT) through regulation of specific signaling pathways. 31,32 Chiang et al reported that the high expression of WISP1 promoted breast cancer cell proliferation, migration, and invasion, and induced EMT, through the downregulation of E-cadherin and upregulation of N-cadherin, Snail, and b-catenin.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of long non-coding RNA CCAT2 suppresses growth and metastasis of esophageal squamous cell carcinoma by inhibiting the β-catenin/WISP1 signaling pathway

Yang

Zhou

et al. 2021

J Int Med Res

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Objective Long non-coding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) plays oncogenic roles in several cancers, including esophageal squamous cell carcinoma (ESCC). However, the specific mechanism of how CCAT2 influences ESCC tumorigenesis is still unknown. Methods Using RT-qPCR, the mRNA expression levels of CCAT2 in 33 paired ESCC and adjacent non-cancer tissues and cell lines were measured. Lentiviral vector sh-CCAT2 was designed and transfected into TE10 cells. CCK-8 and transwell assays were employed to detect the effects of CCAT2 knockdown on cell proliferation and invasion, respectively. RT-qPCR and western blots were used to detect the effects of CCAT2 knockdown. Results CCAT2 was overexpressed in ESCC tissues compared with corresponding adjacent tissues. CCAT2 knockdown could suppress cell proliferation and invasion in vitro. Furthermore, knockdown of CCAT2 could suppress the mRNA and protein levels of β-catenin and Wnt-induced-secreted-protein-1 (WISP1), as well as the mRNA levels of their downstream targets VEGF-A, MMP2, and ICAM-1. High expression of CCAT2 and WISP1 were associated with poor prognosis of ESCC patients. Conclusions In conclusion, a novel CCAT2/β-catenin/WISP1 axis was revealed in ESCC progression and may provide a promising therapeutic target against ESCC. CCAT2 and WISP1 are potential molecular biomarkers for predicting prognosis of ESCC.

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“…As a result, WISP1 is a dual-acting molecule with an oncogenic effect in some tumors and suppressor in others [40]. Low levels in melanoma increased tumor progression [33], while high levels in lung and prostate cancer suppressed invasion and metastasis [40].…”

Section: Discussionmentioning

confidence: 99%

Serum WNT-induced secreted protein 1 level as a potential biomarker for thyroid nodules

Duman

Sariakçali

2021

Mìžnarodnij endokrinologìčnij žurnal

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Background. Thyroid nodule (TN) is a common thyroid disease worldwide, and it has increased significantly last decades. Most TNs are usually incidental findings of asymptomatic, benign lesions discovered by imaging modalities performed for reasons unrelated to thyroid diseases. The purpose of this study was to investigate the value of serum WNT-induced secreted protein 1 (WISP1) level as a supporting biomarker to perform differential diagnosis of benign and non-benign thyroid nodules. Materials and methods. The study was completed with the 89 patients undergone fine needle aspiration biopsy and 43 controls. The patients were composed of 96 (72.7 %) females and 36 (27.3 %) males. And they were divided into 2 group according to the Bethesda cytological evaluation as Benign (Bethesda 2) and Non-Benign (Bethesda 3–6) groups. Their serum WISP1 levels were measured by an ELISA method. Results. There were 58 (43.9 %) patients in Benign (Bethesda 2) and 31 (23.5 %) in non-Benign (Bethesda 3–6) groups. In the contrary nodule size was bigger in the Non-benign group than that benign group (p = 0.006). The serum WISP1 level in the Benign (Bethesda 2) group was significantly higher than that in the and Non-Benign (Bethesda 3–6) group, and controls (p < 0). The difference between benign and non-benign group accordingly to their echogenicitiy was significant (p < 0.05). In benign group there was 76.9 % mixed echoic nodules, 76.7 % isoechoic nodules 68.4 % isohypoechoic nodules and 35.7 % hypoechoic nodules. In the non-benign group, the highest hypoechoic echo (64.3 %), the least mixed echo (23.1 %), while in the benign group, the most mixed echo (76.9 %), the least hypoechoic echo (35.7 %) was present. There was no relation between WISP1 levels and echogenicity with Kruskal-Wallis H test. Conclusions. According to the preliminary results of current study, addition of serum WISP1 measurement to the differential diagnostic work-up of thyroid nodules patients may provide supportive information. In thyroid nodules patients with Benign (Bethesda 2) category of cytological evaluation, a higher level of serum WISP1 may support cytological diagnosis.

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Dual effect of WISP-1 in diverse pathological processes

Cited by 14 publications

References 48 publications

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

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

Knockdown of long non-coding RNA CCAT2 suppresses growth and metastasis of esophageal squamous cell carcinoma by inhibiting the β-catenin/WISP1 signaling pathway

Serum WNT-induced secreted protein 1 level as a potential biomarker for thyroid nodules

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