WWC3 Inhibits Glioma Cell Proliferation Through Suppressing the Wnt/β-Catenin Signaling Pathway

Wang, Yanni; Jiang, Man; Yao, Yongshan; Cai, Zhengwei

doi:10.1089/dna.2017.3931

Cited by 24 publications

(19 citation statements)

References 24 publications

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“…Downregulation of WWC3 is associated with poor prognosis of cancer patients. 28 , 29 , 30 WWC3 inhibits cell proliferation and metastasis through regulating the Hippo and Wnt signaling pathways. 28 , 29 , 30 , 31 In our present study, linear WWC3 was associated with good prognosis and inhibited breast cancer cell growth and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“… 28 , 29 , 30 WWC3 inhibits cell proliferation and metastasis through regulating the Hippo and Wnt signaling pathways. 28 , 29 , 30 , 31 In our present study, linear WWC3 was associated with good prognosis and inhibited breast cancer cell growth and metastasis. However, the circular form of WWC3 was dominant and exhibited oncogenic functions in breast cancer, indicating that the competition of circWWC3 with the linear WWC3 promoted the progression of breast cancer.…”

Section: Discussionmentioning

confidence: 99%

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ZEB1-Mediated Transcriptional Upregulation of circWWC3 Promotes Breast Cancer Progression through Activating Ras Signaling Pathway

Meng

Liu

et al. 2020

Molecular Therapy - Nucleic Acids

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Zinc finger E-box binding homeobox 1 (ZEB1) has been widely recognized as an important driver of tumor growth and metastasis. However, nothing is known about ZEB1-regulated circular (circ)RNAs in cancer. In the current study, we evaluated the function of a novel ZEB1-regulated circRNA derived from the WWC3 gene locus, circWWC3 in breast cancer progression. We found that ZEB1 upregulated circWWC3 expression but not the linear WWC3 mRNA expression. circWWC3 is highly expressed in breast cancer tissues and is associated with the poor prognosis of breast cancer patients. Silencing of circWWC3 significantly suppresses the proliferation, migration, and invasion of breast cancer cells. Mechanically, circWWC3 upregulates multiple oncogenes’ expression of the Ras signaling pathway through acting as the sponge of microRNA (miR)-26b-3p and miR-660-3p. Moreover, short hairpin (sh)RNA-mediated knockdown of circWWC3 partially antagonized ZEB1-mediated breast cancer growth and metastasis in vivo . Our findings reveal that ZEB1-mediated upregulation of circWWC3 promotes breast cancer progression through activating Ras signaling pathway, which provides a potential therapeutic target and prognostic biomarker for breast cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

ZEB1-Mediated Transcriptional Upregulation of circWWC3 Promotes Breast Cancer Progression through Activating Ras Signaling Pathway

Meng

Liu

et al. 2020

Molecular Therapy - Nucleic Acids

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“…The WW and C2 domain-containing protein (WWC) family serves important roles in regulating cell proliferation, cell migration and synaptic signaling. The overexpression of WWC3 inhibits glioma cell proliferation, migration and invasion (24).…”

Section: Discussionmentioning

confidence: 99%

Identification of hub genes and pathways in glioblastoma by bioinformatics analysis

Yang

Gao

2018

Oncol Lett

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Glioblastoma (GBM) is the most common type of malignant brain tumor, and is associated with poor patient prognosis. A comprehensive understanding of the molecular mechanism underlying GBM may help to guide the identification of novel diagnoses and treatment targets. The gene expression profile of the GSE4290 GBM dataset was analyzed in order to identify differentially expressed genes (DEGs). Enriched pathways were identified through Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes analyses. A protein-protein interaction network was constructed in order to identify hub genes and for module analysis. Expression and survival analyses were conducted in order to screen and validate critical genes. A total of 1,801 DEGs were recorded, including 620 upregulated and 1,181 downregulated genes. Upregulated DEGs were enriched in the terms ‘mitotic cell cycle process’, ‘mitotic cell cycle’ and ‘cell cycle process’. Downregulated genes were enriched in ‘transsynaptic signaling’, ‘anterograde transsynaptic signaling’ and ‘synaptic signaling’. A total of 15 hub genes, which displayed a high degree of connectivity, were selected. These genes included vascular endothelial growth factor A, cyclin-dependent kinase 1 (CDK1), cell-division cycle protein 20 (CDC20), aurora kinase A (AURKA), and budding uninhibited by benzimidazoles 1 (BUB1). The identified DEGs and hub genes may help guide investigations on the mechanisms underlying the development and progression of GBM. CDK1, CDC20, AURKA and BUB1, which are involved in cell cycle pathways, may be potential targets in the diagnosis and therapy of GBM.

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“…CTNNB1 gene (Gene ID: 1499), also named β-catenin, and glycogen synthase kinase 3 beta (GSK3B, Gene ID: 2932) gene are two pivotal effectors in Wnt/CTNNB1 signaling pathway. Accumulating evidences showed Wnt/CTNNB1 signaling pathway was activated frequently during tumorigenesis and progress of glioma 18,19. Nevertheless, the interaction between Wnt/CTNNB1 signaling pathway and SNHG5 in glioma was poorly demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of long non-coding RNA SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway

Hu¹,

Hong²,

Shang³

2019

J. Cancer

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Objective : Human brain glioma is the most malignant primary intracranial tumor, which has poor prognosis and high mortality. Long noncoding RNAs are considered to take part in cellular phenotypes and are emerging as diagnostic and prognostic biomarkers of glioma. This study will research the effects of Small Nucleolar RNA Host Gene 5 (SNHG5) gene on malignant cellular phenotypes in glioma and explore the possible mechanisms. Materials and Methods : The expression level of SNHG5 was examined using quantitative Real-time PCR in glioma tissues and cell lines. Loss-of-function experiments of SNHG5 together with Enhanced Cell Counting Kit-8, flow cytometry and cell invasion assay were used to investigate the effects of SNHG5 on malignant cellular phenotypes of glioma cells. Finally, luciferase assay and western blotting were applied to determine the activity of WNT/CTNNB1 signaling pathway. Results : SNHG5 gene was high-expressed in glioma tissues and cell lines. Knockdown of SNHG5 gene depressed cell proliferation and invasiveness as well as promoted the apoptosis of U251 and U87 cells. In addition, online database analysis showed SNHG5 was closely related to Wnt/CTNNB1 signaling pathway. Knockdown of SNHG5 inactivated Wnt/CTNNB1 signaling pathway, and the activating of Wnt/CTNNB1 signaling pathway partly restored the influences of SNHG5 knockdown on malignant cellular phenotypes of U251 and U87 cells. Conclusion : SNHG5 gene was high-expressed in glioma, knockdown of SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway.

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WWC3 Inhibits Glioma Cell Proliferation Through Suppressing the Wnt/β-Catenin Signaling Pathway

Cited by 24 publications

References 24 publications

ZEB1-Mediated Transcriptional Upregulation of circWWC3 Promotes Breast Cancer Progression through Activating Ras Signaling Pathway

ZEB1-Mediated Transcriptional Upregulation of circWWC3 Promotes Breast Cancer Progression through Activating Ras Signaling Pathway

Identification of hub genes and pathways in glioblastoma by bioinformatics analysis

Knockdown of long non-coding RNA SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway

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