MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial–mesenchymal transition in anaplastic thyroid cancer cells

Zhang, Xiaoping; Liu, Lin; Deng, Xianzhao; Li, Dan; Cai, Haidong; Ma, Yu‐Shui; Jia, Chengyou; Wu, Bo; Fan, Youben; Lv, Zhongwei

doi:10.1038/s41388-018-0447-1

Cited by 47 publications

(50 citation statements)

References 57 publications

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“…Additionally, miRNA upregulation can promote thyroid cancer EMT. The results of a recent study show that miR-483-3p plays a role in regulating the PARD3 polarity gene in ATC, thus enhancing the EMT process (58). Indeed, miR-483-3p is highly expressed in ATC cell lines, and it can be induced via TGFβ treatment to target PARD3 mRNA.…”

Section: Tgfβ and Mirnas In Emt Regulationmentioning

confidence: 99%

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Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Fuziwara

Saito

Kimura

2019

Archives of Endocrinology and Metabolism

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Thyroid cancer has been rapidly increasing in prevalence among humans in last 2 decades and is the most prevalent endocrine malignancy. Overall, thyroid-cancer patients have good rates of long-term survival, but a small percentage present poor outcome. Thyroid cancer aggressiveness is essentially related with thyroid follicular cell loss of differentiation and metastasis. The discovery of oncogenes that drive thyroid cancer (such as RET, RAS, and BRAF), and are aligned in the MAPK/ERK pathway has led to a new perspective of thyroid oncogenesis. The uncovering of additional oncogenemodulated signaling pathways revealed an intricate and active signaling cross-talk. Among these, microRNAs, which are a class of small, noncoding RNAs, expanded this cross-talk by modulating several components of the oncogenic network-thus establishing a new layer of regulation. In this context, TGFβ signaling plays an important role in cancer as a dual factor: it can exert an antimitogenic effect in normal thyroid follicular cells, and promote epithelial-to-mesenchymal transition (EMT), cell migration, and invasion in cancer cells. In this review, we explore how microRNAs influence the loss of thyroid differentiation and the increase in aggressiveness of thyroid cancers by regulating the dual function of TGFβ. This review provides directions for future research to encourage the development of new strategies and molecular approaches that can improve the treatment of aggressive thyroid cancer.

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Section: Tgfβ and Mirnas In Emt Regulationmentioning

confidence: 99%

“…Blocking miR-483-3p using antagomirs inhibits TGFβ-induced cell invasion and prevents PARD3 downregulation. Interestingly, PARD3 rescue in ATC cells leads to the blockage of TGFβ-induced effects via the maintenance of E-cadherin levels and the inhibition of vimentin (58).…”

Section: Tgfβ and Mirnas In Emt Regulationmentioning

confidence: 99%

Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Fuziwara

Saito

Kimura

2019

Archives of Endocrinology and Metabolism

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“…Recently, emerging studies have suggested that many other lncRNAs, such as PTCSC3 and HCP5, were dysregulated in ATC tissues and cells, implying that they might be promising biomarkers for ATC diagnosis [11,36]. Moreover, a group of miRNAs, including miR-19a and miR-483-3p, were reported to be involved in ATC progression, suggesting novel therapeutic targets for ATC treatment [37,38]. This study had led to a novel identification for the NEAT1/ miR-206 and NEAT1/miR-599 axis that might function as valuable diagnostic biomarkers and therapeutic targets for ATC management in further personalized medicine.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA NEAT1 suppresses hypoxia-induced migration, invasion and glycolysis in anaplastic thyroid carcinoma cells through regulation of miR-206 and miR-599

et al. 2020

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Background: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal malignancies. Long noncoding RNAs (lncRNAs) are being found to play crucial roles in ATC progression. Herein, we focused on the role of nuclear paraspeckle assembly transcript 1 (NEAT1) on ATC progression under hypoxia and underlying mechanisms governing it. Methods: The expression levels of NEAT1, miR-206 and miR-599 were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell migration and invasion abilities were detected using transwell assays. Glucose consumption and lactate production were determined using a corresponding commercial assay kit. Western blot was performed to evaluate the level of hexokinase 2 (HK2). The targeted interplays between NEAT1 and miR-206 or miR-599 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft model was established to observe the effect of NEAT1 on tumor growth in vivo. Results: Our data indicated that NEAT1 was highly expressed in ATC tissues and cells, and hypoxia induced NEAT1 expression in ATC cells. NEAT1 depletion repressed ATC cell migration, invasion and glycolysis under hypoxia. Mechanistically, NEAT1 acted as a molecular sponge of miR-206 and miR-599. Moreover, the repressive effects of NEAT1 knockdown on ATC cell migration, invasion and glycolysis under hypoxia were mediated by miR-206 or miR-599. Additionally, NEAT1 knockdown weakened tumor growth in vivo. Conclusion: In conclusion, our study suggested that a low NEAT1 expression suppressed the migration, invasion, and glycolysis in ATC cells under hypoxia at least partially through modulating miR-206 and miR-599, providing new therapeutic strategies for ATC treatment.

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“…19,20 In fact, it has been reported that a variety of miRNAs can function as biomarkers for the diagnosis and prognosis of human gliomas. 21 In recent years, miR-483 has been demonstrated to be downregulated in colon cancer, hepatocellular carcinoma and gastric cancer, 9,12,22 while it was upregulated in anaplastic thyroid cancer and Wilms' Tumor, 23,24 suggesting that the expression of miR-483 is distinct in different types of cancers. In this study, we found that miR-483 was low expressed in glioma tissues compared to the paracancerous normal tissues.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-483 Targeted SOX3 to Suppress Glioma Cell Migration, Invasion and Promote Cell Apoptosis</p>

Lu¹,

Yu²,

Zhang³

et al. 2020

OTT

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Objective: Glioma is the most common malignant brain tumor that has high aggressiveness. The aim of this study was to investigate the potential therapeutic targets for gliomas. Materials and Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to calculate the expression of miRNA and genes. The connection between the expression of miR-483 and patients' overall survival rate was evaluated using Kaplan-Meier analysis. In addition, the underlying mechanism was detected using luciferase assay. Results: The expression level of miR-483 was significantly decreased in glioma tissue samples and cell lines, compared to the adjacent tissues and normal cell lines. Downregulation of miR-483 or upregulation of SOX3 was associated with overall survival of glioma patients. Additionally, overexpression of miR-483 promotes cell invasion and migration and inhibits apoptosis. In addition, miR-483 directly targeted to SOX3, and the expression of miR-483 has a negative correlation with SOX3 in glioma tissues. SOX3 reversed partial functions of miR-483 on cell migration, invasion, and promoted cell apoptosis in glioma. Conclusion: MiR-483 inhibited glioma cell migration, invasion, and promoted glioma cell apoptosis by targeting SOX3. MiR-483 maybe acted as a potential target for the treatment of glioma.

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MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial–mesenchymal transition in anaplastic thyroid cancer cells

Cited by 47 publications

References 57 publications

Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Interplay of TGFβ signaling and microRNA in thyroid cell loss of differentiation and cancer progression

Knockdown of lncRNA NEAT1 suppresses hypoxia-induced migration, invasion and glycolysis in anaplastic thyroid carcinoma cells through regulation of miR-206 and miR-599

<p>MiR-483 Targeted SOX3 to Suppress Glioma Cell Migration, Invasion and Promote Cell Apoptosis</p>

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