MicroRNA-33b Suppresses Migration and Invasion by Targeting c-Myc in Osteosarcoma Cells

Xu, Nuo; Li, Zimu; Yu, Zhange; Yan, Feng; Liu, Yang; Lu, Xiaofeng; Yang, Wenjing

doi:10.1371/journal.pone.0115300

Cited by 59 publications

(53 citation statements)

References 34 publications

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“…7F and G). To further define the mechanistic link between mevalonate and MYC, we examined mevalonate regulation of a miR previously reported to regulate MYC levels, miR-33b (33, 34). After statin therapy, miR-33b expression levels increased in vitro (Fig.…”

Section: Resultsmentioning

confidence: 99%

MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor–Initiating Cells

et al. 2017

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Metabolic dysregulation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastomas with wildtype IDH are poorly understood. MYC promotes metabolic reprogramming in cancer, but targeting MYC has proven notoriously challenging. Here, we link metabolic dysregulation in patient-derived brain tumor initiating cells (BTICs) to a nexus between MYC and mevalonate signaling, which can be inhibited by statin or 6-fluoromevalonate treatment. BTICs preferentially express mevalonate pathway enzymes, which we find regulated by novel MYC binding sites, validating an additional transcriptional activation role of MYC in cancer metabolism. Targeting mevalonate activity attenuated RAS-ERK-dependent BTIC growth and self-renewal. In turn, mevalonate created a positive feed-forward loop to activate MYC signaling via induction of miR-33b. Collectively, our results argue that MYC mediates its oncogenic effects in part by altering mevalonate metabolism in glioma cells, suggesting a therapeutic strategy in this setting.

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Section: Resultsmentioning

confidence: 99%

MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor–Initiating Cells

et al. 2017

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“…Currently, the mechanisms responsible for the oncogenic insults in the initiation and progression of osteosarcoma remain to be fully elucidated. To date, a number of miRNAs have been determined to be deregulated in osteosarcoma and to participate in osteosarcoma development, including miR-212 (8), miR-33b (9), miR-503 (10) and miR-451 (11). In addition, the present authors also reported that miR-143 and miR-133a are downregulated in osteosarcoma, and they function as anti-oncomiRs in osteosarcoma development (12,13).…”

Section: Introductionmentioning

confidence: 99%

Increased expression of microRNA-148a in osteosarcoma promotes cancer cell growth by targeting PTEN

Zhang

Wang

et al. 2016

Oncology Letters

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Osteosarcoma is the most common type of primary malignant bone tumor, and deregulated microRNAs (miRNAs or miRs) in osteosarcoma have attracted great attention. In the present study, through miRNA microarray analysis, it was identified that miR-148a expression was significantly increased in osteosarcoma tissues. Increased miR-148a expression was significantly correlated with tumor progression and prognosis. Furthermore, increased miR-148a expression could promote osteosarcoma growth in vitro and in vivo, and the tumor-promoting effect was due to enhanced activation of the phosphoinositide 3-kinase signaling pathway caused by miR-148a-mediated inhibition of phosphatase and tensin homolog expression. Together, the present results suggest a role for miR-148a in osteosarcoma development and its potential use in prognosis prediction and cancer therapy.

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“…21 The family of miR-33 contains miR-33a and mir-33b, which are encoded in the SREBP gene intron. [23][24][25][26] However, the role of miR-33b on the sensitivity to DNR in AML cells remains unclear. 22 miR-33b can be used as a tumor suppressor by inhibiting cell proliferation in various human cancers, such as breast cancer, lung cancer, melanoma, colorectal cancer, and osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐33b regulates sensitivity to daunorubicin in acute myelocytic leukemia by regulating eukaryotic translation initiation factor 5A‐2

Liu

Lei

Qiao

et al. 2019

J of Cellular Biochemistry

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In this study, we aimed to study the effect of miR‐33b in regulating sensitivity to daunorubicin (DNR) in acute myelocytic leukemia (AML). We used quantitative real‐time polymerase chain reaction and Cell Counting Kit‐8 assay to detect the level of miR‐33b and cell viability. Cell apoptosis and the expression of eIF5A‐2 and MCL‐1 protein were detected by flow cytometry analysis and Western Blot analysis, respectively. MiR‐33b mimic increased sensitivity of AML cells against DNR, while miR‐33b inhibitor had the opposite effect. Furthermore, the results showed that the eIF5A‐2 gene was a direct target of miR‐33b, and miR‐33b regulated eIF5A‐2 mRNA and protein expression. Silencing of eIF5A‐2 by RNA interference increased the sensitivity of AML cells against DNR. We also found that MCL‐1 contributed to the regulation of DNR sensitivity, which was dependent on downregulation of eIF5A‐2. Finally, knockdown of eIF5A‐2 eliminated the effects of miRNA‐33b mimic or inhibitor on DNR sensitivity. These findings indicate that miR‐33b maybe as a new therapeutic target in AML cells.

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MicroRNA-33b Suppresses Migration and Invasion by Targeting c-Myc in Osteosarcoma Cells

Cited by 59 publications

References 34 publications

MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor–Initiating Cells

MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor–Initiating Cells

Increased expression of microRNA-148a in osteosarcoma promotes cancer cell growth by targeting PTEN

MicroRNA‐33b regulates sensitivity to daunorubicin in acute myelocytic leukemia by regulating eukaryotic translation initiation factor 5A‐2

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