miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Zhao, Xuefeng; Xu, Yan; Sun, Xiaoya; Ma, Yuan; Zhang, Yan; Wang, Yadong; Guan, Hongya; Jia, Zhen; Li, Yuebai; Wang, Yisheng

doi:10.1002/jcb.27832

Cited by 21 publications

(18 citation statements)

References 26 publications

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“…To further elucidate the ceRNA network, considering that functional miRNA is known to regulate its target gene expression, the potential target of miR-17-5p was explored by bioinformatics analysis. Previous studies have revealed transforming growth factor-β receptor 2, SRC kinase signaling inhibitor 1, phosphatase and tensin homologue and cyclin-dependent kinase inhibitor 1 as functional targets of miR-17-5p in multiple conditions [10][11][12]. In this study, as indicated by luciferase reporter assay, we identified TLR4 as a target of miR-17-5p, which is also consistent with a previous report [17].…”

Section: Discussionsupporting

confidence: 92%

“…miRNAs also serve as regulator of inflammatory response and have essential roles in diagnosis and treatment of sepsis [9]. miR-17-5p has been shown to have an impact on the outcome of various disorders [10][11][12]. More particularly, miR-17-5p has been suggested as an inflammation-related miRNA and might be associated with sepsis-induced acute lung injury [13,14].…”

Section: Introductionmentioning

confidence: 99%

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NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

Guo

Cai

2020

Open Medicine

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AbstractBackgroundThe inflammatory response of macrophages is responsible for sepsis. Long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to be involved in sepsis development. However, its underlying mechanism remains largely unclear. This study aims to investigate the effect of NEAT1 on inflammatory response of macrophages and explore the regulatory network of NEAT1/microRNA-17-5p (miR-17-5p)/Toll-like receptor 4 (TLR4).MethodsThe serum samples of 68 sepsis patients and 32 heathy controls were collected. THP-1 macrophages were treated with lipopolysaccharide (LPS) to induce inflammatory injury model of sepsis. The expressions of NEAT1, miR-17-5p and TLR4 were measured by quantitative real-time polymerase chain reaction or western blot. The inflammatory response was investigated by levels of inflammatory cytokines, tumor necrosis factor-alpha (TNF-ɑ), interleukin-1beta (IL-1β) and IL-6 as well as nitric oxide (NO) production. The interaction among NEAT1, miR-17-5p and TLR4 were investigated by bioinformatics analysis, luciferase reporter assay and RNA pull-down.ResultsNEAT1 expression was enhanced in patient serum and associated with severity of sepsis. Knockdown of NEAT1 inhibited levels of TNF-ɑ, IL-1β, IL-6 and NO release in LPS-treated macrophages. miR-17-5p is bound to NEAT1 and its abrogation reversed NEAT1 knockdown-mediated inhibition of inflammatory response in LPS-treated macrophages. Overexpression of miR-17-5p weakened LPS-induced inflammatory response. TLR4 as a target of miR-17-5p was regulated by NEAT1 and miR-17-5p. TLR4 res-to ration alleviated silencing NEAT1-induced inflammatory suppression.ConclusionSilence of NEAT1 suppressed LPS-induced inflammatory response of macrophages by mediating miR-17-5p and TLR4, indicating that NEAT1 might be a promising target for sepsis treatment.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

Guo

Cai

2020

Open Medicine

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“…MiRNA supplementary therapy has become one promising strategy for the treatment of different types of thyroid cancer [18]. MiR-17-5p, as an attractive miRNA, has been reported to serve as an important oncogene in human cancers, such as osteosarcoma, cervical cancer, nasopharyngeal, breast cancer, pancreatic cancer and gastric cancer [8][9][10][19][20][21]. However, its role in thyroid cancer remains largely unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Cai et al provided evidence that miR-17-5p promoted cell proliferation and metastasis via regulating transforming growth factor-β receptor 2 (TGFBR2) in cervical cancer [9]. In addition, miR-17-5p could induce proliferation and epithelial-mesenchymal transition by inhibiting SRC kinase signaling inhibitor 1 in osteosarcoma [10]. Previous study demonstrated that miR-17-5p is highly expressed in thyroid cancer [11].…”

mentioning

confidence: 99%

miR-17-5p knockdown inhibits proliferation, autophagy and promotes apoptosis in thyroid cancer via targeting PTEN

Shi¹,

Liu²,

Li³

et al. 2020

neo

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Thyroid cancer is one common endocrine malignancy with various pathological types. MicroRNAs (miRNAs) play essential roles in development, prognosis and treatment of thyroid cancer. However, the role of miR-17-5p in thyroid cancer progression and its mechanism remain poorly understood. The expressions of miR-17-5p and phosphatase and tensin homolog (PTEN) were measured in thyroid cancer tissues and cells by quantitative real-time polymerase chain reaction or western blot. Cell proliferation and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and flow cytometry, respectively. The protein levels of biomarkers in autophagy or protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway were analyzed by western blot. The interaction between miR-17-5p and PTEN was probed by luciferase activity assay. We found that miR-17-5p expression was elevated and PTEN level was reduced in thyroid cancer tissues and cells compared with their corresponding controls. Knockdown of miR-17-5p or overexpression of PTEN suppressed cell proliferation and autophagy but promoted apoptosis in thyroid cancer cells. PTEN was indicated as a target of miR-17-5p and its interference reversed abrogation of miR-17-5p-mediated inhibition of proliferation and autophagy and increase of apoptosis. Moreover, downregulation of miR-17-5p impeded the activation of AKT/mTOR pathway in thyroid cancer cells, which was attenuated by silencing PTEN. Our data supported that knockdown of miR-17-5p upregulated PTEN expression, therefore leading to suppression of the malignancy of thyroid cancer and inactivation of AKT/mTOR pathway, providing a novel avenue for treatment of thyroid cancer.

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“…Furthermore, classic EMT markers such as N-cadherin, E-cadherin and Snail were quantified by western blot analysis. Finally, it was proven that SRCIN1 is a direct target of miR-17-5p and silencing of this miRNA could change the expression of EMT markers and arrest cell growth (76). SRCIN1 was found to be downregulated in breast cancer in previous studies (77).…”

Section: Mirna-mediated Src Oncogenic Signaling In Selected Cancer Typesmentioning

confidence: 93%

Historical retrospective of the SRC oncogene and new perspectives (Review)

et al. 2020

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Since its first discovery as part of the Rous sarcoma virus (RSV) genome, the c-SRC (SRC) proto-oncogene has been proved a key regulator of cancer development and progression, and thus it has been highlighted as an attractive target for anti-cancer therapeutic strategies. Though the exact mechanisms of its action are still not fully understood, SRC protein mediates crucial normal cell functions, such as cell development, proliferation and survival, and its dysregulation is considered as an oncogenic signature and a driving force for cancer initiation. In the present review, we present a flashback to the history of the Src research, while focusing on the most important milestones in the field. Moreover, we investigate the proposed regulatory mechanisms and molecules that mediate its action in order to designate putative therapeutic targets and useful prognostic and/or diagnostic tools. Furthermore, we present and discuss existing therapeutic approaches that are explored in clinical settings. Contents 1. Introduction 2. Discovery of Rous sarcoma virus 3. Cellular origin of retroviral oncogenes 4. MicroRNAs as the fine tuners of SRC oncogenic signaling 5. miRNA-mediated SRC oncogenic signaling in selected cancer types 6. Exosomes as the fine tuners of oncogenic signaling 7. SRC inhibitors as anticancer agents in clinical trials 8. Conclusion

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miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1

Cited by 21 publications

References 26 publications

NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

miR-17-5p knockdown inhibits proliferation, autophagy and promotes apoptosis in thyroid cancer via targeting PTEN

Historical retrospective of the SRC oncogene and new perspectives (Review)

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