LncRNA BDNF‐AS inhibits proliferation, migration, invasion and EMT in oesophageal cancer cells by targeting miR‐214

Zhao, Huaying; Diao, Changying; Wang, Xiaohui; Xie, Yilin; Liu, Yaqing; Gao, Xiao‐Ning; Li, Shenglei

doi:10.1111/jcmm.13558

Cited by 33 publications

(17 citation statements)

References 29 publications

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“…These branched CDH1 + tubules in 2D cultures are more likely to represent ureteric bud derivatives and inhibiting miR-214-3p could, thus, favor ureteric bud epithelium stabilization, while restricting MM (as shown by the reduction in WT1 + cells). In agreement with this interpretation, CDH1 itself has been previously reported as a direct target of miR-214 ( Wang et al., 2016 ), while in some cancers miR-214 was found to promote EMT ( Liu et al., 2018a ; Long et al., 2015 ; Zhao et al., 2018 ) and therefore inhibiting it would be expected to result in epithelial stabilization.…”

Section: Discussionsupporting

confidence: 75%

The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model

et al. 2021

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Summary MicroRNAs (miRNAs) are gene expression regulators and they have been implicated in acquired kidney diseases and in renal development, mostly through animal studies. We hypothesized that the miR-199a/214 cluster regulates human kidney development. We detected its expression in human embryonic kidneys by in situ hybridization. To mechanistically study the cluster, we used 2D and 3D human embryonic stem cell (hESC) models of kidney development. After confirming expression in each model, we inhibited the miRNAs using lentivirally transduced miRNA sponges. This reduced the WT1 + metanephric mesenchyme domain in 2D cultures. Sponges did not prevent the formation of 3D kidney-like organoids. These organoids, however, contained dysmorphic glomeruli, downregulated WT1 , aberrant proximal tubules, and increased interstitial capillaries. Thus, the miR-199a/214 cluster fine-tunes differentiation of both metanephric mesenchymal-derived nephrons and kidney endothelia. While clinical implications require further study, it is noted that patients with heterozygous deletions encompassing this miRNA locus can have malformed kidneys.

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Section: Discussionsupporting

confidence: 75%

The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model

et al. 2021

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“…Several lines of evidence suggested that lncRNA BDNF‐AS was remarkably downregulated in a variety of tumour cells with its level of expression being correlated with cancer aggressiveness and inhibited tumorigenesis by regulating cell proliferation, migration, invasion, and apoptosis. For example, lncRNA BDNF‐AS was significantly decreased in oesophageal cancer tissues and cells; besides, lncRNA BDNF‐AS upregulation reduced oesophageal cancer cell proliferation, migration, and invasion as well as epithelial‐to‐mesenchymal transition (EMT) . Forced expression of lncRNA BDNF‐AS in human retinoblastoma cells inhibited cell proliferation and migration and induced cell‐cycle arrest .…”

Section: Discussionmentioning

confidence: 62%

LncRNA BDNF‐AS suppresses colorectal cancer cell proliferation and migration by epigenetically repressing GSK‐3β expression

Zhi

Lian

2019

Cell Biochemistry & Function

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This study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA (lncRNA) brain‐derived neurotrophic factor antisense (BDNF‐AS) in colorectal cancer (CRC). The quantitative real‐time PCR (qRT‐PCR) and western blotting were performed to detect the expressions of lncRNA BDNF‐AS and glycogen synthase kinase‐3β (GSK‐3β) in human CRC tissues and cell lines. The cell proliferation, transwell migration, and invasion assays were carried out to evaluate the effect of lncRNA BDNF‐AS on the growth of CRC cells. RNA pull‐down and RNA immunoprecipitation (RIP) assays were conducted to confirm the interaction between lncRNA BDNF‐AS and enhancer of Zeste Homologue 2 (EZH2). Chromatin immunoprecipitation (ChIP) assay was used to verify the enrichment of EZH2 and histone H3 lysine 27 trimethylation (H3K27me3) in the promoter region of GSK‐3β in CRC cells. LncRNA BDNF‐AS expression was significantly decreased, while GSK‐3β was highly expressed in human CRC tissues and cell lines. Moreover, lncRNA BDNF‐AS induced inhibition of proliferation, migration, and invasion of CRC cells via inhibiting GSK‐3β expression. Mechanistically, BDNF‐AS led to GSK‐3β promoter silencing in CRC cells through recruitment of EZH2. In conclusion, lncRNA BDNF‐AS functioned as an oncogene in CRC and shed new light on lncRNA‐directed therapeutics in CRC. Significance of the study LncRNA BDNF‐AS is recently reported to be remarkably downregulated in a variety of tumours and served as a tumour suppressor. However, the functions and underlying mechanism of lncRNA BDNF‐AS in CRC pathogenesis have not been reported yet. Our study is the first to demonstrate the effect of lncRNA BDNF‐AS in CRC and revealed that lncRNA BDNF‐AS expression is negatively correlated with the aggressive biological behaviour of CRC. Further investigation demonstrated that lncRNA BDNF‐AS functioned as a tumour suppressor in CRC progression by suppressing GSK‐3β expression through binding to EZH2 and H3K27me3 with the GSK‐3β promoter, shedding light on the diagnosis and therapy for CRC.

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“…Recent studies have shown that the EMT program is closely linked to tumor metastasis. 35,36 Notably, EMT markers, including E-cad (marker of epithelial cells), N-cad and VIM (markers of mesenchymal cells), are regulated by the ERK1/2 signaling pathway in pancreatic cancer. [37][38][39][40] In the current study, we indicated that ApoE2 activated ERK1/2 signaling to promote the expression of N-cad and VIM at both the mRNA and protein levels while reducing the expression of E-cad.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein E2 Promotes the Migration and Invasion of Pancreatic Cancer Cells via Activation of the ERK1/2 Signaling Pathway

Wang¹,

Du²,

Cai³

et al. 2020

CMAR

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Background Apolipoprotein E2 (ApoE2) is reported to be essential for cell metastasis and proliferation and has been considered a potential diagnostic marker in many cancers. However, the function of ApoE2 in the metastasis of pancreatic cancer, as well as the underlying mechanism, remain unclear. Purpose In this study, we explored the effect of ApoE2 on the migration and invasion abilities of pancreatic cancer cells and explored the underlying molecular mechanism. Methods and Results Wound healing and Matrigel Transwell assays were used to investigate the role of ApoE2 in cell migration and invasion. Western blotting analysis showed that ApoE2 was overexpressed in pancreatic cancer tissues. Additionally, the overexpression of ApoE2 promoted the process of epithelial–mesenchymal transition (EMT) and enhanced the expression of MMP-2/9 in pancreatic cancer cells. Mechanistically, we found that inhibition of ERK1/2 signaling with PD98059 impaired the ApoE2-mediated promotion of cell migration, invasion and EMT. Conclusion This study demonstrated that ApoE2/ERK1/2 signaling promoted the migration and invasion of pancreatic cancer cells. ApoE2 might be a potential therapeutic target for the treatment of pancreatic cancer metastasis.

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LncRNA BDNF‐AS inhibits proliferation, migration, invasion and EMT in oesophageal cancer cells by targeting miR‐214

Cited by 33 publications

References 29 publications

The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model

The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model

LncRNA BDNF‐AS suppresses colorectal cancer cell proliferation and migration by epigenetically repressing GSK‐3β expression

Apolipoprotein E2 Promotes the Migration and Invasion of Pancreatic Cancer Cells via Activation of the ERK1/2 Signaling Pathway

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