Estrogen-related receptor α participates transforming growth factor-β (TGF-β) induced epithelial-mesenchymal transition of osteosarcoma cells

Chen, Yantao; Zhang, Kun-Shui; Li, Yang; He, Qing

doi:10.1080/19336918.2016.1221567

Cited by 31 publications

(27 citation statements)

References 33 publications

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“…Thus, we focused on transcription factors binding to the MALAT1 promoter. We selected TGF-β because Chen et al [ 24 ] found that TGF-β functioned as a potent stimulator of osteosarcoma cell epithelial-mesenchymal transition. As expected, TGF-β mRNA expression was significantly increased in osteosarcoma tissues compared with the paired noncancerous tissues (Figure 3A ).…”

Section: Resultsmentioning

confidence: 99%

MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2

Huo

Wang

et al. 2017

Oncotarget

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Osteosarcoma is the most common type of bone cancer, especially in children and young adults. Recently, long noncoding RNAs (lncRNAs) have emerged as new prognostic markers and gene regulators in several cancers, including osteosarcoma. In this study, we investigated the contributions of the lncRNA MALAT1 in osteosarcoma with a specific focus on its transcriptional regulation and its interaction with EZH2. Our results showed that MALAT1 was significantly increased in osteosarcoma specimens and cell lines. ROC curve analysis showed that MALAT1 had a higher area under the curve than alkaline phosphatase, and Kaplan-Meier survival analysis indicated that patients with high serum levels of MALAT1 showed reduced survival rate. Knockdown of MALAT1 decreased osteosarcoma cell invasion and promoted E-cadherin expression. Mechanistic investigations showed that MALAT1 was transcriptionally activated by TGF-β. Additionally, EZH2 is highly expressed and associated with the 3’ end region of lncRNA MALAT1 in osteosarcoma, and this association finally suppressed the expression of E-cadherin. Subsequently, our gain and loss function assay showed that MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown. In conclusion, our work illuminates that lncRNA MALAT1 is a potential diagnostic and prognostic factor in osteosarcoma and further demonstrates how MALAT1 confers an oncogenic function. Thus, lncRNA MALAT1 may serve as a promising prognostic and therapeutic target for osteosarcoma patients.

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Section: Resultsmentioning

confidence: 99%

MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2

Huo

Wang

et al. 2017

Oncotarget

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“…Similarly, in malignant bone tumors, osteosarcomas, elevated levels of ZEB1 are detected compared to normal bone and ZEB1 expression is higher in metastatic osteosarcoma in comparison with the group without metastases (Shen et al ., ). A recent study shows that TGF‐β treatment can trigger MT of osteosarcoma cells in vitro involving estrogen‐related receptor α‐dependent activation of SNAI1 (Chen et al ., ). Thus, MT may be involved in the onset and progression of sarcomas but more studies are required for further substantiation.…”

Section: Emt‐ and Met‐related Processes In Sarcomasmentioning

confidence: 97%

EMT‐ and MET‐related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities

2017

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The epithelial‐to mesenchymal (EMT) process is increasingly recognized for playing a key role in the progression, dissemination, and therapy resistance of epithelial tumors. Accumulating evidence suggests that EMT inducers also lead to a gain in mesenchymal properties and promote malignancy of nonepithelial tumors. In this review, we present and discuss current findings, illustrating the importance of EMT inducers in tumors originating from nonepithelial/mesenchymal tissues, including brain tumors, hematopoietic malignancies, and sarcomas. Among these tumors, the involvement of mesenchymal transition has been most extensively investigated in glioblastoma, providing proof for cell autonomous and microenvironment‐derived stimuli that provoke EMT‐like processes that regulate stem cell, invasive, and immunogenic properties as well as therapy resistance. The involvement of prominent EMT transcription factor families, such as TWIST, SNAI, and ZEB, in promoting therapy resistance and tumor aggressiveness has also been reported in lymphomas, leukemias, and sarcomas. A reverse process, resembling mesenchymal‐to‐epithelial transition (MET), seems particularly relevant for sarcomas, where (partial) epithelial differentiation is linked to less aggressive tumors and a better patient prognosis. Overall, a hybrid model in which more stable epithelial and mesenchymal intermediates exist likely extends to the biology of tumors originating from sources other than the epithelium. Deeper investigation and understanding of the EMT/MET machinery in nonepithelial tumors will shed light on the pathogenesis of these tumors, potentially paving the way toward the identification of clinically relevant biomarkers for prognosis and future therapeutic targets.

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“…During EMT, epithelial cells reorganize their cytoskeleton to alter cell polarity and morphology, and lose their junctions, which increases the invasive capacity of the cells. The hallmarks of EMT include decreased expression of E-cadherin and overexpression of Vimentin [19,20]. In recent years, it was observed that EMT is closely related to carcinoma progression, and acts as a major driver of cellular morphogenesis and tumor progression [21].…”

Section: Introductionmentioning

confidence: 99%

FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells

Gao

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cell surface morphology plays pivotal roles in malignant progression and epithelial-mesenchymal transition (EMT). Previous research demonstrated that microvilli play a key role in cell migration of non-small cell lung cancer (NSCLC). In this study, we report that Forkhead box class O1 (FOXO1) is downregulated in human NSCLC and that silencing of FOXO1 is associated with the invasive stage of tumor progression. Methods: The cell proliferation, migration, and invasion were characterized in vitro, and we tested the expression of the Epithelial-mesenchymal transition (EMT) marker by immunofluorescence staining and also identified the effect of FOXO1 on the microvilli by scanning electron microscopy (SEM). Results: Functional analyses revealed that silencing of FOXO1 resulted in an increase in NSCLC cell proliferation, migration, and invasion; whereas overexpression of FOXO1 significantly inhibited the migration and invasive capability of NSCLC cells in vitro. Furthermore, cell morphology imaging showed that FOXO1 maintained the characteristics of epithelial cells. Immunofluorescence staining and western blotting showed that the E-cadherin level was elevated and Vimentin was reduced by FOXO1 overexpression. Conversely, the E-cadherin level was reduced and Vimentin was elevated in cells silenced for FOXO1. Furthermore, scanning electron microscopy (SEM) showed that FOXO1 overexpression increased the length of the microvilli on the cell surface, whereas FOXO1 silencing significantly reduced their length. Conclusions: FOXO1 is involved in human lung carcinogenesis and may serve as a potential therapeutic target in the migration of human lung cancer.

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Estrogen-related receptor α participates transforming growth factor-β (TGF-β) induced epithelial-mesenchymal transition of osteosarcoma cells

Cited by 31 publications

References 33 publications

MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2

MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2

EMT‐ and MET‐related processes in nonepithelial tumors: importance for disease progression, prognosis, and therapeutic opportunities

FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells

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