Lnc<scp>RNA</scp>‐<scp>FENDRR</scp> mediates <scp>VEGFA</scp> to promote the apoptosis of brain microvascular endothelial cells via regulating miR‐126 in mice with hypertensive intracerebral hemorrhage

Dong, Baizhuo; Zhou, Bin; Huang, Shengming; Han, Liang; Nie, Honghua; Chen, Guohui; Liu, Shibing; Zhang, Yanna; Bao, Ning; Yang, Xiaolong; Feng, Hongwei

doi:10.1111/micc.12499

Cited by 37 publications

(23 citation statements)

References 38 publications

(58 reference statements)

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“…In this study, we focused on the function and mechanism of FENDRR in CML cells based on its higher expression in K562/ADM cells. Actually, there have been few reports about FENDRR in different cancers [35][36][37][38]. Zhang et al reported that FENDRR was decreased in human prostate cancer tissues.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

Zhang

Li³

et al. 2019

FEBS Letters

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Chemotherapy is a major anticancer therapeutic modality, however, multidrug resistance (MDR) is frequently observed and hinders treatment efficacy. Here, we investigated the role and potential mechanism of the long noncoding RNA (lncRNA) FENDRR in adriamycin resistance of chronic myeloid leukaemia (CML) cells. FENDRR overexpression attenuates adriamycin resistance, as shown by increased Rhodamine 123 accumulation, promotion of cell apoptosis in vitro and suppression of tumour growth in vivo. Mechanistically, we identified that FENDRR reduces the interaction of the RNA‐binding protein HuR with MDR1 via acting as a sponge, and miR‐184 competitively binds to FENDRR with HuR. Thus, the HuR/FENDRR/miR‐184 interaction contributes to MDR1 activity. These findings indicate that FENDRR is a potential target for reversing adriamycin resistance.

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Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

Zhang

Li³

et al. 2019

FEBS Letters

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“…For example, lncRNA APTR elevated the progression of OS via suppression of miR‐132‐3p . Besides, lncRNA‐FENDRR elevated apoptosis of brain microvessels via regulating miR‐126 in hypertensive intracerebral hemorrhage mice . LncRNA ATB promoted proliferation, migration, and incursion of bladder cancer through inhibiting miR‐126 .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126

Song

Feng

Gao

et al. 2019

J of Cellular Biochemistry

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Peripheral artery disease (PAD) is a serious hazard to the elderly in the lower extremity atherosclerotic plaque, accompanied by a large number of angiogenesis. Long noncoding RNA Alu-mediated p21 transcriptional regulator (APTR) exerts important functions in promoting cell growth. Therefore, we planned to research the mechanism of APTR in angiogenesis in PAD. CCK-8 assay, flow cytometry analysis, and migration assay were to detect cell viability, apoptosis, and migration respectively. The interaction between APTR and miR-12 was tested through luciferase activity test. In vitro angiogenesis assay was used to test the number of tubular cells. qRT-PCR and Western blot were to test expression of APTR, miR-126, and angiogenesis relative factors. There was spontaneously pipe-formation in HEMC-1 cells under matrigel condition. Knockdown of APTR inhibited cell viability and migration and reduced the number of tubular cells. Further, APTR sponged miR-126 and downregulating miR-126 to promote angiogenesis. Overexpression of APTR promoted cell activity and migration and increased the number of tubular cells via negatively regulating miR-126. APTR could elevate activating phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal-regulated kinase signal pathways via negatively regulating miR-126 to promote cell proliferation, migration, and pipe-formation. We researched the mechanism of angiogenesis that APTR elevated proliferation, migration, and pipe-formation via negatively regulating miR-126. K E Y W O R D SAlu-mediated p21 transcriptional regulator (APTR), angiogenesis, miR-126How to cite this article: Song A, Feng R, Gao J, Yang C. LncRNA APTR promotes proliferation, migration, and pipe-formation of human microvascular endothelial cells by sponging miR-126.

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“…Emerging evidence has revealed the important roles of FENDRR in cell differentiation and tumor progression. FENDRR could promote the apoptosis of human brain microvascular endothelial cells via miR-126 regulating VEGFA in hypertensive intracerebral hemorrhage [17]. Yan Li et al revealed that FENDRR has low expression in breast cancer cell lines and cancerous tissues, and inhibits cell proliferation, promotes cell apoptosis, and is associated with good prognosis in breast cancer [14].…”

Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

Qin

Zhou

et al. 2019

Cell Cycle

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This study was to investigate the biological function and underlying mechanisms of FENDRR in cholangiocarcinoma (CCA) cell proliferation, migration and invasion. FENDRR and survivin expression in CCA tissues or cell lines were measured by qRT-PCR. In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blotting. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blotting. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K9 methylation, thereby represses CCA cell proliferation, migration and invasion. ARTICLE HISTORY

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LncRNA‐FENDRR mediates VEGFA to promote the apoptosis of brain microvascular endothelial cells via regulating miR‐126 in mice with hypertensive intracerebral hemorrhage

Abstract: FENDRR could promote the apoptosis of HBMECs via miR-126 regulating VEGFA in HICH.

Cited by 37 publications

References 38 publications

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

LncRNA FENDRR attenuates adriamycin resistance via suppressing MDR1 expression through sponging HuR and miR‐184 in chronic myelogenous leukaemia cells

Retracted: Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

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