The Tumor-Suppressor WWOX and HDAC3 Inhibit the Transcriptional Activity of the β-Catenin Coactivator BCL9-2 in Breast Cancer Cells

El-Hage, Perla; Petitalot, Ambre; Monsoro-Burq, Anne H.; Maczkowiak, Frédérique; Driouch, Keltouma; Formstecher, Étienne; Camonis, Jacques; Sabbah, Michèle; Bièche, Ivan; Lidereau, Rosette; Lallemand, François

doi:10.1158/1541-7786.mcr-14-0180

Cited by 13 publications

(17 citation statements)

References 45 publications

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“…It has been reported that BCL9L induces early phases of human intestinal cancer progress by regulating the β-catenin function switch between adhesion and transcription (Brembeck et al, 2004;Huge et al, 2020). Moreover, BCL9L is demonstrated to enhance β-catenin-mediated transcriptions and increase the abilities of proliferation and metastasis in breast and colon cancer cell lines (Brembeck et al, 2011;El-Hage et al, 2015). However, the effects of BCL9L in osteosarcoma has never been clearly reported, and the relationship between the miR-766-3p/BCL9L axis and β-catenin signal pathway involved in OS is still subject to intense investigation.…”

Section: Introductionmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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Accumulating evidence has indicated that abnormal microRNAs (miRNAs) serve critical roles in carcinogenesis and development of osteosarcoma (OS). The purpose of the present study was to elucidate the relationship between miR-766-3p and development of osteosarcoma and explore the potential mechanism. In this study, we found that miR-766-3p was the most downregulated miRNA by analyzing GSE65071 from the GEO database. miR-766-3p was lowly expressed in OS tissue samples and cells, and high miR-766-3p expression repressed the malignant level of OS, including cell proliferation, EMT, migration, and invasion in vitro and in vivo. B-Cell Lymphoma 9-Like Protein (BCL9L) was negatively associated with miR-766-3p expression in OS cells and tissue samples and was validated as the downstream target by luciferase reporter assay and western blotting. Rescue experiment indicated that BCL9L could restore the influence of miR-766-3p on OS cells. In addition, the β-Catenin/TCF-4 signal pathway was demonstrated to be related to the miR-766-3p/BCL9L axis. In summary, miR-766-3p, a negative regulator of BCL9L, plays the role of tumor metastasis suppressor via the β-catenin signaling pathway in the progression of OS.

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Section: Introductionmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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“…BCL9L was shown to promote tumor progression of breast cancer (25, 46), choriocarcinoma (26), pancreatic cancer (27), and colon cancer (28, 29). Data from pancreatic cancer cells confirm that BCL9L depletion leads to inhibition of EMT (27).…”

Section: Discussionmentioning

confidence: 99%

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

Sun

Liu²,

Lin

et al. 2019

FASEB j.

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The epithelial‐mesenchymal transition (EMT) is crucial for cancer progression. Evidence has shown that miR‐22 and miR‐214 play a key role in colon cancer progression; however, the underlying mechanism remains to be known. The effects of miR‐22 and miR‐214 on EMT are contradictory in different cancers, and whether miR‐22 and miR‐214 are involved in the colon cancer EMT process needs to be elucidated. In this study, we evaluated the exact role and the regulation mechanism of miR‐22 and miR‐214 in colon cancer. After transfection with miR‐22 expression vector, the cell proliferation and migration capacity of HCT116 and RKO cells were significantly suppressed. Also, E‐cadherin was increased and vimentin was decreased by miR‐22 overexpression. Similar effects were also observed after miR‐214 expression vector transfection. Dual‐lucif erase reporter confirmed that BCL9L is the target gene of both miR‐22 and miR‐214. Silencing of BCL9L inhibits cell proliferation and migration, and the expression of E‐cadherin and vimentin was also altered by BCL9L knockdown, which was consistent with miR‐22 or miR‐214 transfection. Furthermore, miR‐22 and miR‐214 inhibited tumor growth in nude mice. Moreover, although the association between BCL9L's lower expression and longer survival time was statistically nonsignificant, a trend existed; further studies in a larger cohort are needed. Collectively, these data suggest that miR‐22 and miR‐214 inhibit cell proliferation, migration, and EMT of colon cancer, most likely by targeting BCL9L.—Sun, R., Liu, Z., Han, L., Yang, Y., Wu, F., Jiang, Q., Zhang, H., Ma, R., Miao, J., He, K., Wang, X., Zhou, D., Huang, C. miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signliang in colon cancer. FASEB J. 33, 5411–5424 (2019). http://www.fasebj.org

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“… 16 , 20 – 22 It has been found to regulate gene transcription by sequestering transcription factors in the cytoplasm, thus limiting their access to the cell nucleus and target genes, 23 , 24 and there is also one report indicating that WWOX may interact with transcription factor complex directly in nucleus. 25 …”

Section: Introductionmentioning

confidence: 99%

The WWOX gene in brain development and pathology

Kośla

Kałuzińska

2020

Exp Biol Med (Maywood)

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Shortly after its discovery in 2000, WWOX was hailed as a tumor suppressor gene. In subsequent years of research, this function was confirmed indisputably. Majority of tumors show high rate of loss of heterozygosity and decreased expression of WWOX. Nevertheless, over the years, the range of its known functions, at the cellular, organ and system levels, has expanded to include metabolism and endocrine system control and CNS differentiation and functioning. Despite of its function as a tumor suppressor gene, WWOX genetic alternations were found in a number of metabolic and neural diseases. A lack of WWOX protein as a consequence of germline mutations results in brain development disturbances and malfunctions. Impact statement WW domain-containing oxidoreductase encoded by the WWOX gene is a transcription regulator and a key player in a number of cellular and biological processes such as tumor suppression, cell proliferation, apoptosis induction, steroid metabolism, and central nervous system development. This review provides a comprehensive summary of currently known roles and discusses the importance of WWOX gene for CNS development and functioning.

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The Tumor-Suppressor WWOX and HDAC3 Inhibit the Transcriptional Activity of the β-Catenin Coactivator BCL9-2 in Breast Cancer Cells

Cited by 13 publications

References 45 publications

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

miR‐22 and miR‐214 targeting BCL9L inhibit proliferation, metastasis, and epithelial‐mesenchymal transition by down‐regulating Wnt signaling in colon cancer

The WWOX gene in brain development and pathology

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