<scp>RUNX</scp>3 is down‐regulated in glioma by Myc‐regulated miR‐4295

Li, Xinxing; Zheng, Jihui; Diao, Hongyu; Liu, Yunhui

doi:10.1111/jcmm.12736

Cited by 15 publications

(14 citation statements)

References 36 publications

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“…17 Propranolol has been used to treat high blood pressure, a number of types of irregular heart rate, thyrotoxicosis, and capillary hemangiomas. [20][21][22][23] However, the effect of miR-4295 has not been studied in IH. 2 MicroRNA-4295 (miR-4295) is one of the important miRNAs, which participates in mediating various biological processes, including cell proliferation, apoptosis, migration, and invasion.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Propranolol suppresses HUVEC viability, migration, VEGF expression, and promotes apoptosis by downregulation of miR‐4295

Zhao

Yang

et al. 2018

J of Cellular Biochemistry

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Infantile hemangioma (IH) is a common benign tumor. Human umbilical vein endothelial cells (HUVECs) have the potential of stem cells, which has been widely used in vascular endothelial cell experiments. Oral propranolol was first reported to treat hemangioma in 2008. However, the role of propranolol in IH remains unclear. Therefore, in this study, we investigated the effects of propranolol on HUVECs in vitro, to explore the underlying mechanism of propranolol in IH. HUVECs were treated with 0.15, 1.5, and 15 μM of propranolol, and transfected with microRNA‐4295 (miR‐4295) mimic. Cell viability, migration, and apoptosis were examined using Cell Counting Kit‐8, transwell assay, and flow cytometry analysis, respectively. In addition, the expressions and concentrations of miR‐4295, vascular endothelial growth factor (VEGF), VEGF‐A, FLT1, FLT2, and FOXF1 were assessed using real‐time polymerase chain reaction, Western blot assay, and enzyme‐linked immunosorbent assay. We found that 15 μM of propranolol decreased HUVEC viability the most. Then, cell migration and the concentrations of VEGF and VEGF‐A were reduced, and apoptosis was increased when treated with propranolol. Meanwhile, the expressions of VEGF, VEGF‐A, FLT1, FLT2, and FOXF1 were downregulated by propranolol exposure. Further study showed that miR‐4295 expression was upregulated in IH tissues, and propranolol treatment downregulated miR‐4295 expression in HUVECs. MiR‐4295 overexpression alleviated the reductions of viability, migration, and factors expression, as well as the increase of apoptosis. Propranolol suppressed HUVEC viability, migration, the expression of VEGF, VEGF‐A, FLT1/2, FOXF1, and promoted apoptosis via downregulation of miR‐4295. This study lays a foundation for further study of the effect of propranolol on IH.

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Section: Introductionmentioning

confidence: 99%

Retracted: Propranolol suppresses HUVEC viability, migration, VEGF expression, and promotes apoptosis by downregulation of miR‐4295

Zhao

Yang

et al. 2018

J of Cellular Biochemistry

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“…Intriguingly, we identified miR‐4295, an oncogenic miRNA, as a PTPN14‐targeting miRNA. Numerous studies have demonstrated that miR‐4295 expression is increased in various tumours, and it functions as a oncogenic miRNA that promotes the proliferation and invasion of tumour cells 45‐47 . In line with these reports, our study elucidated that miR‐4295 expression was increased in osteosarcoma tissues and cell lines.…”

Section: Discussionsupporting

confidence: 86%

PTPN14, a target gene of miR‐4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling

Liang

Duan

et al. 2020

Clin Exp Pharma Physio

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Non-receptor tyrosine phosphatase 14 (PTPN14) has emerged as a novel tumoursuppressor in a wide range of human cancer types. However, the role of PTPN14 in osteosarcoma remains undetermined. In the present study, we aimed to explore the expression pattern, biological function, and regulation of PTPN14 in osteosarcoma.Low PTPN14 expression levels were detected in osteosarcoma cells, and PTPN14 overexpression markedly decreased the proliferation, colony formation, and invasive potential of osteosarcoma cells. Bioinformatics analysis predicted PTPN14 as a potential target gene of microRNA-4295 (miR-4295), and this prediction was validated by a dual-luciferase reporter assay. PTPN14 expression was negatively modulated by miR-4295 in osteosarcoma cells. Moreover, PTPN14 expression was inversely correlated with miR-4295 expression in osteosarcoma tissues. Notably, miR-4295 inhibition significantly restricted the proliferation and invasion of osteosarcoma cells. PTPN14 overexpression or miR-4295 inhibition increased the phosphorylation ofYes-associated protein 1 (YAP1) and impeded YAP1 nuclear translocation, leading to inhibition of YAP1-mediated transcriptional activity. However, the miR-4925-inhibition-mediated antitumour effect was partially reversed by PTPN14 knockdown.Overall, these results demonstrate that PTPN14 is a miR-4295 target gene and it exerts a tumour-suppressive function in osteosarcoma cells via inactivation of YAP1.Our study uncovers a miR-4295-PTPN14-YAP1 signalling pathway that may play a crucial role in the progression of osteosarcoma. K E Y W O R D S miR-4295, osteosarcoma, PTPN14, YAP1 S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Liang G, Duan C, He J, Ma W, Dai X. PTPN14, a target gene of miR-4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling.

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“…Dysregulation of microRNAs is connected with various cancer sub-types, including GC ( 31 ). Overexpression of miR-4295 in glioma tissue was also reported, and its level was revealed to be associated with clinical stage ( 32 ). Furthermore, the present study identified that LRIG1 was a downstream target gene of miR-4295, and that LRIG1 was downregulated in GC cells.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-4295 enhances cisplatin-induced gastric cancer cell apoptosis through the EGFR/PI3K/Akt signaling pathway by targeting LRIG1

Yan

Yuan

et al. 2018

Int J Oncol

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Gastric cancer (GC) is one of the leading causes of cancer-associated mortality worldwide. The aim of the present study was to investigate the mechanism of microRNA-4295 (miR-4295), which regulates cisplatin (DDP)-induced apoptosis in GC cells through the leucinerich repeats and immunoglobulin-like domains 1 (LRIG1)-mediated epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Two cell lines were selected, one with the highest expression of miR-4295 and one with the lowest expression of LRIG1, for the experiments. The half maximal inhibitory concentration of DDP in the human GC MKN-28 and MKN-45 cell lines was calculated, and mitochondrial membrane potentials of the GC cells were detected by tetramethylrhodamine, ethyl ester, perchlorate staining. The proliferation and apoptosis of GC cells with or without DDP treatment were assessed by MTT assay and plate colony formation, as well as flow cytometry and TUNEL staining. Western blot analysis and reverse transcription-quantitative polymerase chain reaction were employed to determine the expression of EGFR/PI3K/Akt signaling pathway-related genes and apoptosis-related genes. LRIG1 was identified as a target gene of miR-4295. The expression of miR-4295 was upregulated, and the expression of LRIG1 was downregulated in GC cells. Furthermore, DDP enhanced the decrease in miR-4295 expression and the increase in LRIG1 expression in GC cells. miR-4295 promoted the proliferation and inhibited the DDP-induced apoptosis of GC cells without DDP treatment. In addition, miR-4295 increased the expression levels of EGFR, PI3K, Akt, p-PI3K and p-Akt, suggesting that miR-4295 promotes the activation of the EGFR/PI3K/Akt signaling pathway by targeting LRIG1. miR-4295 targeted and negatively regulated LRIG1 expression to activate the EGFR/PI3K/Akt signaling pathway, thereby promoting the proliferation of the GC cells and inhibiting the apoptosis of the GC cells induced by DDP. Therefore, miR-4295 may be a novel therapeutic target in patients with GC.

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RUNX3 is down‐regulated in glioma by Myc‐regulated miR‐4295

Cited by 15 publications

References 36 publications

Retracted: Propranolol suppresses HUVEC viability, migration, VEGF expression, and promotes apoptosis by downregulation of miR‐4295

Retracted: Propranolol suppresses HUVEC viability, migration, VEGF expression, and promotes apoptosis by downregulation of miR‐4295

PTPN14, a target gene of miR‐4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling

Downregulation of microRNA-4295 enhances cisplatin-induced gastric cancer cell apoptosis through the EGFR/PI3K/Akt signaling pathway by targeting LRIG1

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