A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report

Grassilli, Silvia; Nika, Ervin; Lambertini, Elisabetta; Brugnoli, Federica; Piva, Roberta; Capitani, Silvano; Bertagnolo, Valeria

doi:10.1007/s13402-016-0292-6

Cited by 15 publications

(30 citation statements)

References 35 publications

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“…It has been reported that VAV1 was expressed in a neuroblastoma cell line SK‐N‐MC and exerted influence on the development of neuroblastomas . A previous study revealed that miR‐142‐3p had negative effects on VAV1 expression, and miR‐142‐3p was important for the agonist‐induced expression of VAV1 and PU.1 . MiR‐499‐5p was reported to be a candidate target of VAV3 and miR‐499‐5p could suppress VAV3 expression in non‐small cell lung cancer cells .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Zhou

Wang

et al. 2018

J of Cellular Biochemistry

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This study aims to explore the effect of miR-330 targeting VAV1 on amyloid β-protein (Aβ) production, oxidative stress (OS), and mitochondrial dysfunction in Alzheimer's disease (AD) mice through the MAPK signaling pathway. Putative targeted gene of miR-330 was performed by a miRNA target prediction website and dual-luciferase reporter gene assay. AD mouse model was successfully established. Fourteen C57 mice were randomized into AD and control groups. The positive protein expression rate of VAV1 was measured by immunohistochemistry. Neuron cells were assigned into control, blank, negative control (NC), miR-330 mimics, miR-330 inhibitors, siRNA-VAV1, and miR-330 inhibitors + siRNA-VAV1 groups. Expression of miR-330, VAV1, ERK1, JNK1, P38MAPK, Aβ, COX, and lipoprotein receptor-related protein-1 (LRP-1) were determined using RT-qPCR and Western blotting. Colorimetry was applied to measure the levels of OS parameters of superoxide dismutase (SOD) and malondialdehyde (MDA). Aβ production in brain tissue was detected using ELISA, while that in neuron cell was measured by radioimmunoassay. MiR-330 was down-regulated in neuron cells of AD mice and VAV1 was negatively regulated by miR-330. Compared with the control group, the positive protein expression rate of VAV1 was significantly elevated in the AD group. Overexpression of miR-330 decreased the expression of VAV1, ERK1, JNK1, P38MAPK, and Aβ, but increased the expression of COX and LRP-1. AD mice revealed elevated Aβ production and MDA with decreased SOD level. The result indicates that overexpressed miR-330 targeting VAV1 through the MAPK signaling pathway reduces Aβ production and alleviates OS and mitochondrial dysfunction in AD.

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Section: Discussionmentioning

confidence: 99%

Retracted: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Zhou

Wang

et al. 2018

J of Cellular Biochemistry

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“…Wang et al indicated that miR-142-3p was a key regulator of normal myeloid differentiation and its reduced expression was related to AML development [37], therefore serving as a candidates for AML prognosis and therapeutic strategy [25]. Grassilli et al demonstrated that the existence of Vav1, PU.1 which regulated ATRA-induced gene expression, as well as miR-142-3p, supported ATRA-induced differentiation in APL-derived NB4 cells [38]. Our study confirmed that miR-142-3p was downregulated in AML PBMC and cells, as well as AML/ATRA and AML/ADR cells.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR-142-3p Improves Drug Sensitivity of Acute Myelogenous Leukemia through Reducing P-Glycoprotein and Repressing Autophagy by Targeting HMGB1

Zhang

Liu

2017

Translational Oncology

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miR-142-3p was reported to be downregulated in acute myelogenous leukemia (AML) and acted as a novel diagnostic marker. However, the regulatory effect of miR-142-3p on drug resistance of AML cells and its underlying mechanism have not been elucidated. Here, we found that miR-142-3p was significantly downregulated and high mobility group box 1 (HMGB1) was dramatically upregulated in AML samples and cells, as well as drug-resistant AML cells. P-gp level and autophagy were markedly enhanced in HL-60/ADR and HL-60/ATRA cells. miR-142-3p overexpression improved drug sensitivity of AML cells by inhibiting cell viability and promoting apoptosis, and inhibited P-gp level and autophagy in drug-resistant AML cells, whereas HMGB1 overexpression obviously reversed these effect. HMGB1 was demonstrated to be a target of miR-142-3p, and miR-142-3p negatively regulated HMGB1 expression. In conclusion, our study elucidated that upregulation of miR-142-3p improves drug sensitivity of AML through reducing P-glycoprotein and repressing autophagy by targeting HMGB1, contributing to better understanding the molecular mechanism of drug resistance in AML.

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“…Micro‐dissected tissues were subjected to RNA extraction with miRNeasy FFPE Kit (QIAGEN), following the manufacturer's protocol. RNA was subjected to real‐time PCR for quantitative measurement of miR‐146a using the TaqMan MicroRNA assay (Life Technologies) and a Bio‐Rad CFX96™ system, as previously reported . Fold‐changes were calculated using the 2 −ΔΔCT method and normalized to the expression of U6 snRNA.…”

Section: Methodsmentioning

confidence: 99%

“…For miR‐146a analysis, RNA was subjected to single stranded cDNA synthesis using a TaqMan MicroRNA Reverse Transcription Kit (Life Technologies), according to the manufacturer's instructions. The cDNAs obtained were employed as templates for quantitative Real‐Time PCR, following a previously described procedure …”

Section: Methodsmentioning

confidence: 99%

Ectopic expression of PLC‐β2 in non‐invasive breast tumor cells plays a protective role against malignant progression and is correlated with the deregulation of miR‐146a

Bertagnolo

Grassilli

Volinia

et al. 2019

Molecular Carcinogenesis

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Cells in non‐invasive breast lesions are widely believed to possess molecular alterations that render them either susceptible or refractory to the acquisition of invasive capability. One such alteration could be the ectopic expression of the β2 isoform of phosphoinositide‐dependent phospholipase C (PLC‐β2), known to counteract the effects of hypoxia in low‐invasive breast tumor‐derived cells. Here, we studied the correlation between PLC‐β2 levels and the propensity of non‐invasive breast tumor cells to acquire malignant features. Using archival FFPE samples and DCIS‐derived cells, we demonstrate that PLC‐β2 is up‐regulated in DCIS and that its forced down‐modulation induces an epithelial‐to‐mesenchymal shift, expression of the cancer stem cell marker CD133, and the acquisition of invasive properties. The ectopic expression of PLC‐β2 in non‐transformed and DCIS‐derived cells is, to some extent, dependent on the de‐regulation of miR‐146a, a tumor suppressor miRNA in invasive breast cancer. Interestingly, an inverse relationship between the two molecules, indicative of a role of miR‐146a in targeting PLC‐β2, was not detected in primary DCIS from patients who developed a second invasive breast neoplasia. This suggests that alterations of the PLC‐β2/miR‐146a relationship in DCIS may constitute a molecular risk factor for the appearance of new breast lesions. Since neither traditional classification systems nor molecular characterizations are able to predict the malignant potential of DCIS, as is possible for invasive ductal carcinoma (IDC), we propose that the assessment of the PLC‐β2/miR‐146a levels at diagnosis could be beneficial for identifying whether DCIS patients may have either a low or high propensity for invasive recurrence.

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A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report

Cited by 15 publications

References 35 publications

Retracted: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Retracted: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Upregulation of miR-142-3p Improves Drug Sensitivity of Acute Myelogenous Leukemia through Reducing P-Glycoprotein and Repressing Autophagy by Targeting HMGB1

Ectopic expression of PLC‐β2 in non‐invasive breast tumor cells plays a protective role against malignant progression and is correlated with the deregulation of miR‐146a

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