Promoter hypermethylation of Wnt inhibitory factor-1 in patients with lung cancer

Zheng, Yu; Li, Xia; Jiang, Yiming; Xu, Yufen; Song, Binbin; Zhou, Qiang; Liang, Xiaodong; Yang, Xinmei

doi:10.1097/md.0000000000005433

Cited by 14 publications

(12 citation statements)

References 34 publications

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“…Having indicated the critical role of miR-139-5p in bladder cancer progression, we then searched for the potential gene effector involved in its function. Wnt1, a member from WNT gene family, functioned as an oncogene in several types of cancer [ 35 , 36 ]. Recent study found that Wnt1 expression was significantly higher in cutaneous squamous cell carcinoma samples than in normal skin cells, moreover, Wnt1 expression was correlated with the histopathological differentiation [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt/β-catenin signaling pathway in bladder cancer

Deng

Zhang

et al. 2017

Oncotarget

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Bladder cancer is one of the most common urological malignancy all over the world. Recently, long non-coding RNA (lncRNA) XIST has been identified as an oncogenic gene in several type of cancers. However, the expression level and functional role of XIST in bladder cancer remain largely unknown. In the present study, we found that XIST was significantly up-regulated in bladder cancer tissues and cell lines, and was correlated with poor prognosis of bladder cancer patients. Furthermore, XIST knockdown significantly inhibited bladder cancer cell growth and metastasis in vitro and tumor growth in vivo. We also demonstrated that XIST acted as a competing endogenous RNA for miR-139-5p and repression of miR-139-5p could restore the inhibitory effects on bladder cancer cells induced by XIST shRNA. In addition, we identified that Wnt1 was a direct target of miR-139-5p, and XIST played the oncogenic role in bladder cancer by activating the Wnt/β-catenin signaling pathway. Taken together, our study suggested that lncRNA XIST may serve as a prognostic biomarker and a potential therapeutic target for bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt/β-catenin signaling pathway in bladder cancer

Deng

Zhang

et al. 2017

Oncotarget

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“…In HCC, the Wnt/β-catenin pathway has been demonstrated to promote cell proliferation, invasion and angiogenesis ( 22 ). The WIF1 gene, located on human chromosome 12q14, encodes a secreted protein that inactivates the Wnt/β-catenin signaling pathway by binding to Wnt proteins ( 23 ). In the present study, qPCR, western blot analysis and dual-luciferase reporter assay methods were used to confirm that WIF1 is a downstream target of miR-552.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-552 promotes hepatocellular carcinoma progression by downregulating WIF1

Wang

Chen

et al. 2018

Int J Mol Med

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MicroRNAs (miRNAs/miRs) are involved in the metastasis of hepatocellular carcinoma (HCC). In the present study, it was demonstrated that miR-552 was upregulated in HCC tissues. High miR-552 expression was associated with malignant clinicopathological features and decreased survival rates. The in vitro results indicated that miR-552 overexpression promoted migration, invasion and epithelial-mesenchymal transition in Hep3B cells. However, the knockdown of miR-552 inhibited its oncogenic roles in Huh-7 cells. Additionally, Wnt inhibitory factor 1 (WIF1) was demonstrated to be a direct target of miR-552 in Hep3B and Huh-7 cells. Additional experiments identified that miR-552 promotes β-catenin expression by increasing the phosphorylation of GSK3β at Ser9. In conclusion, the results suggested that miR-552 may promote HCC progression by blocking WIF1-mediated GSK3β dephosphorylation. miR-552 may be a biomarker for predicting the outcomes of patients with HCC.

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“…Wnt signalling plays important roles during the development and progression of cancer, including NSCLC . We previously observed that Zbed3 is overexpressed in NSCLC tissues compared to normal lung tissues and is associated with cancer development .…”

Section: Discussionmentioning

confidence: 99%

“…Wnt signalling plays important roles during the development and progression of cancer, including NSCLC. [1][2][3][4][5][6] We previously observed F I G U R E 8 Treatment with a GSK3β inhibitor abolished Zbed3's ability to increase β-catenin expression and Wnt signalling activity. Western blots show that Zbed3 overexpression increases levels of β-catenin while decreasing levels of phospho-β-catenin in A549 cells, and that this effect is abolished by treating the cells with the GSK3β inhibitor TWS119 (A).…”

Section: Discussionmentioning

confidence: 99%

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Zbed3 promotes proliferation and invasion of lung cancer partly through regulating the function of Axin‐Gsk3β complex

Shi

Zhao

Fan

2018

J Cellular Molecular Medi

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Our previous work showed that Zbed3 is overexpressed in nonsmall cell lung cancer and that down‐regulation of Zbed3 inhibited β‐catenin expression and cancer cell proliferation and invasiveness. Here, we investigated Zbed3's ability to promote lung cancer cell proliferation and invasion and the involvement of the Axin/TPC/glycogen synthase kinase 3β (Gsk‐3β) complex to the response. Coimmunoprecipitation assays showed that wild‐type Zbed3 bound to Axin but a Zbed3 mutant lacking the Axin binding site did not. In A549 and H1299 lung cancer cells, Zbed3 overexpression promoted cancer cell proliferation and invasiveness, as well as Wnt signalling and expression of downstream mediators, including β‐catenin, cyclin D1 and MMP7 (P < 0.05). In contrast, the Zbed3 mutant failed to enhance β‐catenin expression (P > 0.05), and its ability to promote cancer cell proliferation and invasiveness was much less than wild‐type Zbed3 (P < 0.05). The ability of Zbed3 to increase β‐catenin levels was abolished by Axin knockdown in A549 cells (P > 0.05). Similarly, treating the cells with a GSK‐3β inhibitor abolished Zbed3's ability to increase β‐catenin levels and Wnt signalling. These results indicate that Zbed3 enhances lung cancer cell proliferation and invasiveness at least in part by inhibiting Axin/adenomatous polyposis coli/GSK‐3β‐mediated negative regulation of β‐catenin levels.

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Promoter hypermethylation of Wnt inhibitory factor-1 in patients with lung cancer

Cited by 14 publications

References 34 publications

Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt/β-catenin signaling pathway in bladder cancer

Long non-coding RNA XIST promotes cell growth and metastasis through regulating miR-139-5p mediated Wnt/β-catenin signaling pathway in bladder cancer

MicroRNA-552 promotes hepatocellular carcinoma progression by downregulating WIF1

Zbed3 promotes proliferation and invasion of lung cancer partly through regulating the function of Axin‐Gsk3β complex

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