MicroRNA-519 enhances HL60 human acute myeloid leukemia cell line proliferation by reducing the expression level of RNA-binding protein human antigen R

Huang, Ke-Bin; Dong, Bing-wei; Wang, Yueyue; Tian, Tian V.; Zhang, Biying

doi:10.3892/mmr.2015.4455

Cited by 13 publications

(10 citation statements)

References 29 publications

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“…In this light, it is not surprising that HuR silencing reduced cell growth parameters in both cell lines. These results are coherent with available data on other cellular models; in fact, HuR silencing reduces cell growth of a wide range of cultured cells [ 25 – 28 ].…”

Section: Discussionsupporting

confidence: 90%

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

et al. 2016

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RNA binding proteins (RBPs) play a central role in cell physiology and pathology. Among them, HuR is a nuclear RBP, which shuttles to the cytoplasm to allow its RNA targets processing. HuR over-expression and delocalization are often associated to cell transformation. Numerous cancers display increased HuR protein levels and its high cytoplasmic levels has been associated with a worse prognosis.In our study, we first evaluated HuR expression in normal and cancer thyroid tissues and then evaluated its function in thyroid cell lines. HuR is over-expressed in all thyroid tumor tissues; high cytoplasmic levels are detected in all thyroid carcinomas. HuR silencing decreased cell viability and determined apoptotic cell death, in a non-tumorigenic (Nthy-ori-3.1) and a tumorigenic (BCPAP) thyroid cell line. Global transcriptome analysis indicated that HuR silencing, though having similar biological effects, induces distinct gene expression modifications in the two cell lines. By using the RIP-seq approach, the HuR-bound RNA profiles of different thyroid cell lines were evaluated. We show that in distinct cell lines HuR-bound RNA profiles are different. A set of 114 HuR-bound RNAs distinguishing tumorigenic cell lines from the non-tumorigenic one was identified.Altogether, our data indicate that HuR plays a role in thyroid tumorigenesis. Moreover, our findings are a proof of concept that RBP targets differ between cells with the same origin but with distinct biological behavior.

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Section: Discussionsupporting

confidence: 90%

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

et al. 2016

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“…Huang et al . showed that miR-519 enhanced cell proliferation and induced cell apoptosis in AML HL-60 cell line by decreasing the level of RNA-binding protein human antigen R [14]. MiR-34a is the first identified tumor suppressor gene that is lower expressed in many forms of tumors, including breast cancer, lung cancer and AML [15-17].…”

Section: Introductionmentioning

confidence: 99%

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

Liu

Ren

Chen

2017

Cell Physiol Biochem

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Background: MiR-34a is identified as a tumor suppressor gene and involved in acute myeloid leukemia (AML) development. However, the regulatory mechanism of miR-34a in AML is unclear. Methods: The expression of miR-34a and HMGB1 in HL-60, THP-1 and HS-5 cells were detected by qRT-PCR and western blot. Lipofectamine 2000 was used to transfect with miR-34a mimics, miR-34a inhibitor, si-HMGB1, pcDNA 3.1-HMGB1, and corresponding controls. The apoptosis and autophagy of transfected AML cells were assessed by flow cytometry and western blot, respectively. Bioinformatics software and dual luciferase reporter assay were applied to predict and verify the target of miR-34a. The effects of miR-34a mimics or si-HMGB1 on chemotherapy-induced autophagy were further explored in HL-60 cells treated with all-trans retinoic acid (ATRA) along with lysosomal protease inhibitors E64d and pepstatin A. Results: MiR-34a was lower expressed and HMGB1 mRNA and proteins were both higher expressed in HL-60 and THP-1 cells compared with that in HS-5 cells. Higher expression levels of MiR-34 and lower expression levels of HMGB1 both significantly promoted apoptosis and inhibited autophagy in HL-60 and THP-1 cells. Dual luciferase reporter system confirmed that HMGB1 was a potential target of miR-34a. Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by higher expression level of miR-34a. Higher expression level of miR-34a and lower expression level of HMGB1 both inhibited chemotherapy-induced autophagy by stimulating the LC3 conversion. Conclusion: MiR-34a promoted cell apoptosis and inhibited autophagy by targeting HMGB1. Therefore, miR-34a may be a potential promising molecular target for AML therapy.

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“…To date, numerous studies have reported that abnormal expressions of miRNAs are involved in the pathogenesis and development of AL. For example, Huang, et al8 have reported that miR-519 promotes AML HL-60 cell proliferation via downregulating the expression of RNA-binding protein human antigen R. miR-34a could enhance cell apoptosis and suppress autophagy by targeting HMGB1 in AML cells 7. miR-146a has been identified to play a dual oncogenic and anticancer role in leukemia,9 because it is overexpressed in childhood ALL and AML,10 but downregulated in adult AML,11 However, the precise roles of miR-146a in AL and its potential molecular mechanism remain to be further investigated.…”

Section: Introductionmentioning

confidence: 99%

microRNA-146a Promotes Growth of Acute Leukemia Cells by Downregulating Ciliary Neurotrophic Factor Receptor and Activating JAK2/STAT3 Signaling

2019

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PurposeAcute leukemia (AL) is classified as acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). This study aimed to investigate the effect of miR-146a on childhood AL and its underlying molecular mechanisms.Materials and MethodsBone marrow samples were obtained from 39 AL children and 10 non-cancer controls. The expressions of miR-146a and ciliary neurotrophic factor receptor (CNTFR) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in ALL and AML pediatric patients, as well as ALL (Jurkat) and AML (HL-60) cells. Correlations between miR-146a and clinical indicators were explored. A targeting relationship between miR-146a and CNTFR was detected by dual luciferase reporter gene assay. Cell proliferation, apoptosis, migration, and invasion of Jurkat and HL-60 cells were measured by MTT assay, flow cytometry, and transwell assay, respectively. LIF expression was detected by qRT-PCR in Jurkat and HL-60 cells. The expression of p-JAK2, JAK2, p-STAT3, and STAT3 in HL-60 cells was measured by Western blot.ResultsmiR-146a was increased in ALL and AML pediatric patients, while CNTFR was decreased. miR-146a expression was associated with immunophenotype, karyotype, fusion gene, and SIL-TAL1. CNTFR was a target gene of miR-146a. miR-146a could promote cell proliferation, migration, and invasion, as well as inhibit cell apoptosis in Jurkat and HL-60 cells by downregulating CNTFR. Meanwhile, miR-146a inhibited the expression of LIF and activated JAK2/STAT3 pathway by downregulating CNTFR.ConclusionmiR-146a could promote the proliferation, migration, and invasion and inhibit the apoptosis of AL Jurkat and HL-60 cells by downregulating CNTFR and activating the JAK2/STAT3 pathway.

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MicroRNA-519 enhances HL60 human acute myeloid leukemia cell line proliferation by reducing the expression level of RNA-binding protein human antigen R

Cited by 13 publications

References 29 publications

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells

microRNA-146a Promotes Growth of Acute Leukemia Cells by Downregulating Ciliary Neurotrophic Factor Receptor and Activating JAK2/STAT3 Signaling

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