HMGA1 facilitates tumor progression through regulating Wnt/β-catenin pathway in endometrial cancer

Han, Xionggao; Cao, Yanhua; Wang, Kun; Zhu, Guiping

doi:10.1016/j.biopha.2016.05.004

Cited by 34 publications

(27 citation statements)

References 34 publications

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“…Apelin modulates these processes via PI3/Akt signaling pathway [41, 42], and G protein-coupled receptor 55 triggers MAPK cascade [43]. Furthermore, high-mobility group A1 protein is involved in Wnt/β-catenin pathway [44]. SK-MEL-1 melanoma cells proliferation was altered after miR-4286 inhibitor application, which matched the changes in the levels of folylpolyglutamate synthase (FPGS), an enzyme crucial for survival of dividing cells.…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative and Pro-Apoptotic Effects of MiR-4286 Inhibition in Melanoma Cells

et al. 2016

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IntroductionMicroRNAs are essential regulators of gene expression at the post-transcriptional level. Their expression is altered in cancer tissues, and evaluation of these alterations is considered a promising tool used to diagnose and identify prognostic markers.Materials and methodsThe microRNA expression profiles of formalin-fixed, paraffin-embedded melanoma and melanocytic nevi samples were estimated with a microarray and subsequently validated by real-time PCR. Melanoma cells were transfected with miR-4286 inhibitor to evaluate the influence of this microRNA on the viability, proliferation, apoptosis, migration, and invasion of melanoma cells.ResultsThe microarray revealed that the expression of 1,171 microRNAs was altered in melanoma samples compared to melanocytic nevi. Real-time PCR validation experiments found the microRNA expression levels to correspond to the melanoma/melanocytic nevi microarray results. The pathway analysis identified 52 modulated pathways in melanoma. Moreover, the application of miR-4286 inhibitor to BRO melanoma cells resulted in a 2.6-fold increase in the apoptosis rate and a 1.7-fold decrease in the cell proliferation/viability but did not affect the invasiveness and migration of these cells. Furthermore, the use of miR-4286 inhibitor altered the mRNA expression of several miR-4286 gene targets: folylpolyglutamate synthase, RNA polymerase I-specific transcription initiation factor, apelin, G-protein-coupled receptor 55, and high-mobility group A1 protein, which have been implicated in cell proliferation/apoptosis regulation. Lastly, the transiently transfected SK-MEL-1 cells with miR-4286 inhibitor decreased proliferation rate and modulated folylpolyglutamate synthase rates of these cells.ConclusionOur results demonstrate that miR-4286 mediates proliferation and apoptosis in melanoma cells, these findings may represent a novel mechanism underlying these processes.

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Section: Discussionmentioning

confidence: 99%

Antiproliferative and Pro-Apoptotic Effects of MiR-4286 Inhibition in Melanoma Cells

et al. 2016

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“…β‐catenin, as one of the main component of the Wnt/β‐catenin signaling pathway, mainly participates in mediating cell adhesion. Wnt/β‐catenin plays important roles in EMT . It has been reported that enrichment of β‐catenin in nuclear could cause EMT in cancer, and the lower expression of E‐cadherin can lead to accumulation of β‐catenin, and then, β‐catenin in the cytoplasm translocated to the cell nucleus to induce the transcription of EMT related genes .…”

Section: Discussionmentioning

confidence: 99%

“…Wnt pathway is an evolutionarily conserved signaling pathway which regulates cell differentiation, cell fate determination, and cell migration during embryogenesis . Meanwhile, many studies show that Wnt signaling regulates cell motility, migration, differentiation, proliferation, and survival in various types of cancer, including OSCC . In the canonical Wnt signaling pathway, activation of Wnt signaling could lead to nuclear accumulation of β‐catenin, which could cause EMT program .…”

Section: Introductionmentioning

confidence: 99%

Casticin inhibits invasion and proliferation via downregulation of β‐catenin and reversion of EMT in oral squamous cell carcinoma

Xie

Liu

Duan

et al. 2019

J Oral Pathology Medicine

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Background Casticin expresses multiple anti‐cancer activities, whereas the effect of casticin on oral squamous cell carcinoma (OSCC) is still unclear. β‐catenin signaling plays a crucial role in the epithelial‐mesenchymal transition which is closely related to tumorigenesis. Herein, we aimed to study the functions of casticin on invasion and migration of OSCC, and clarify whether the effect of casticin on OSCC has a relationship with β‐catenin signaling. Methods Human OSCC cell lines UM1 and HSC‐3 were treated with different concentrations of casticin. The cell viability was evaluated by MTT and soft agar colony formation. Transwell assay and wound‐healing assay were performed to measure the ability of cell invasion and migration. The protein expression was assessed by Western blotting. Results Casticin displayed inhibitory activities of cell viability, invasion, and migration on OSCC cell lines. Meanwhile, casticin could reverse EMT process and inhibit the expression of β‐catenin in OSCC. Knock‐down or overexpression of β‐catenin could alter the effect of casticin on OSCC. Conclusions Casticin impaired invasion and migration of OSCC by inhibition of β‐catenin and reversal of EMT and could be a potential anti‐cancer bioactive agent.

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“…It has been reported that Wnt/β signaling pathway played an important role in endometrial cancer reviewed by Dellinger et al . Han et al disclosed that HMGA1 promoted tumorigenesis via regulation of Wnt/β‐catenin pathway in endometrial cancer . Wang et al demonstrated that Fibulin‐4 restrained endometrial cancer cell invasion and metastasis via Wnt/β‐catenin signaling pathway .…”

Section: Discussionmentioning

confidence: 99%

Investigations on the mechanism of progesterone in inhibiting endometrial cancer cell cycle and viability via regulation of long noncoding RNA NEAT1/microRNA‐146b‐5p mediated Wnt/β‐catenin signaling

Huang

Zhong

et al. 2018

IUBMB Life

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Progesterone is often used to protect the endometrium and prevent endometrial cancer. An intensive study on its molecular mechanism in endometrial cancer would contribute to the development of more promising therapies. Relevant lncRNAs and mRNAs expression data in endometrial cancer cell line Ishikawa pretreated and post‐treated with progesterone were derived from Gene Expression Omnibus (accession no. GSE29435), and then we analyzed long noncoding RNAs and mRNAs with differential expressions in two different conditions. The Cytoscape software, TargetScan, miRanda, and Human microRNA Disease Database (HMDD) websites were employed. Gene set enrichment analysis (GSEA) was used to determine related Kyoto Encyclopedia of Genes and Genomes pathways alteration in Ishikawa cells treated with progesterone. In addition to bioinformatics analysis, Reverse Transcription‐Polymerase Chain Reaction (RT‐PCR), Western blot, and dual‐luciferase reporter assays were performed. The impact of progesterone on cell propagation and cell cycle was testified by colony formation and flow cytometry analysis. LncRNA nuclear enriched abundant transcript 1 (NEAT1) was the most significantly downregulated lncRNA in endometrial cancer cells treated with progesterone. Lymphoid enhancing factor 1 (LEF1) was positively associated with NEAT1, and eventually hsa_miR‐146b‐5p was validated to target both LEF1 and NEAT1. Wnt/β‐catenin signaling pathway was identified to involve in endometrial cancer. NEAT1 or LEF1 was overexpressed in endometrial cancer cells while downregulated following post‐treatment with progesterone. Conversely, miR‐146b‐5p was notably decreased in Ishikawa cells while upregulated after treatment with progesterone. Downstream gene c‐myc or MMP9 regulated by upstream gene LEF1 in Wnt/β‐catenin signaling pathway was remarkably increased in Ishikawa cells and positively related with NEAT1. Progesterone inhibited cell cycle and viability through regulating NEAT1/miR‐146b‐5p axis via Wnt/β‐catenin signaling pathway. Progesterone exerted suppressive influence on endometrial cancer progression via regulation of lncRNA NEAT1/miR‐146b‐5p‐mediated Wnt/β‐catenin signaling pathway, which might reveal new strategies for developing more effective therapeutics. © 2018 IUBMB Life, 71(1):223–234, 2019

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HMGA1 facilitates tumor progression through regulating Wnt/β-catenin pathway in endometrial cancer

Cited by 34 publications

References 34 publications

Antiproliferative and Pro-Apoptotic Effects of MiR-4286 Inhibition in Melanoma Cells

Antiproliferative and Pro-Apoptotic Effects of MiR-4286 Inhibition in Melanoma Cells

Casticin inhibits invasion and proliferation via downregulation of β‐catenin and reversion of EMT in oral squamous cell carcinoma

Investigations on the mechanism of progesterone in inhibiting endometrial cancer cell cycle and viability via regulation of long noncoding RNA NEAT1/microRNA‐146b‐5p mediated Wnt/β‐catenin signaling

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