Epigenetic modification of miR-141 regulates SKA2 by an endogenous ‘sponge’ HOTAIR in glioma

Bian, Erbao; Ma, Chunchun; He, Xiaoxi; Wang, Chao; Zong, Gang; Wang, Hongliang

doi:10.18632/oncotarget.8895

Cited by 62 publications

(43 citation statements)

References 49 publications

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“…The list of significant biomarkers is growing in an astonishing manner and includes a wide range of molecules such as lncRNAs and microRNAs (e.g. HOTAIR and miR-141), and several DNA repair genes (Boccard et al, 2015;Bian et al, 2016;Reon et al, 2016), which are importantly correlated with genome stability and will be explored in more detail in the next sections. Table 3 summarizes the main DNA repair biomarkers discussed in this review.…”

Section: Glioma Classification and Frequent Genetic Alterationsmentioning

confidence: 99%

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance

et al. 2020

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Glioblastoma (GBM) is the most common and malignant type of primary brain tumor, showing rapid development and resistance to therapies. On average, patients survive 14.6 months after diagnosis and less than 5% survive five years or more. Several pieces of evidence have suggested that the DNA damage signaling and repair activities are directly correlated with GBM phenotype and exhibit opposite functions in cancer establishment and progression. The functions of these pathways appear to present a dual role in tumorigenesis and cancer progression. Activation and/or overexpression of ATRX, ATM and RAD51 genes were extensively characterized as barriers for GBM initiation, but paradoxically the exacerbated activity of these genes was further associated with cancer progression to more aggressive stages. Excessive amounts of other DNA repair proteins, namely HJURP, EXO1, NEIL3, BRCA2, and BRIP, have also been connected to proliferative competence, resistance and poor prognosis. This scenario suggests that these networks help tumor cells to manage replicative stress and treatment-induced damage, diminishing genome instability and conferring therapy resistance. Finally, in this review we address promising new drugs and therapeutic approaches with potential to improve patient survival. However, despite all technological advances, the prognosis is still dismal and further research is needed to dissect such complex mechanisms.

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Section: Glioma Classification and Frequent Genetic Alterationsmentioning

confidence: 99%

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance

et al. 2020

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“…Bian et al revealed that HOTAIR might act as an endogenous “sponge” of miR‐141 and that it regulated the derepression of SKA2. Both overexpression of miR‐141 and knockdown of HOTAIR in a mouse model of human glioma resulted in a significant reduction of tumor growth in vivo . Ke et al demonstrated that the knockdown of the long non‐coding RNA HOTAIR inhibited malignant biological behaviors of human glioma cells via the modulation of miR‐326.…”

Section: Discussionmentioning

confidence: 99%

MiR‐15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells

Sun

Wang

Zhang

et al. 2018

J of Cellular Biochemistry

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Among the malignant tumors of the human central nervous system, gliomas have the highest incidence and recurrence rate. Therefore, exploration of the molecular mechanism that underlies the development and progression of gliomas is of great clinical significance. Many studies have demonstrated that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play important roles in the development and progression of tumors. In the present study, both an RNAhybrid analysis and a dual-luciferase reporter gene assay confirmed that microRNA-15b (miR-15b) binding sites were present in the sequence of HOX transcript antisense RNA (HOTAIR). The present study further demonstrated that miR-15b, HOTAIR, and p53 formed a mutually regulated loop. MiR-15b upregulated the expression of p53 but inhibited the expression of HOTAIR. In addition, miR-15b was able to regulate the expression of HOTAIR through p53. P53 promoted miR-15b expression but inhibited HOTAIR expression. Furthermore, the examination of cell proliferation, apoptosis, and invasion revealed that both miR-15b and p53 inhibited the proliferation and invasion, but promoted the apoptosis, of glioma cells. In contrast, HOTAIR exerted effects that were the opposite of those exerted by miR-15b and p53 on glioma cells. The upregulation of HOTAIR suppressed the inhibitory effects of miR-15b and p53 on cell proliferation and invasion as well as the promoting effect of miR-15b and p53 on apoptosis. Therefore, it can be concluded that miR-15b, HOTAIR, and p53 constitute a regulatory loop that is capable of regulating the growth of glioma cells. This finding provides a new target for the treatment of gliomas.

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“…To explore the mechanism of how HOTAIRM1 functions to repress this process, we have adopted the ceRNA theory here, which emphasizes that lncRNAs act as ceRNAs to impair miRNA activity by sequestering paired miRNAs and facilitate corresponding mRNAs to function without miRNA interference 30,31. In the light of this thought, we have found that miR-3960 and its target mRNA HOXA1 are able to build a ceRNA network with lncRNA HOTAIRM1, which functionally influences DC differentiation.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of long noncoding RNA HOTAIRM1 promotes monocyte/dendritic cell differentiation through competitively binding to endogenous miR-3960

Xin

Feng

et al. 2017

OTT

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Myeloid differentiation is controlled by a multilayered regulatory circuitry consisting of various elements, including histone modifications, transcription factors, and posttranscriptional regulators such as miRNAs, long noncoding RNAs, and circular RNAs. However, the molecular mechanism underlying this biological process remains unclear. In this study, through epigenetic profiling analysis using chromatin immunoprecipitation (ChIP) followed by sequencing (ChIP-seq), we identified an lncRNA, HOTAIRM1, with a critical role in myeloid development. Further ChIP-chip analysis showed obvious H3K4me3 and H3K27me3 histone modification peak changes in the promoter region of HOTAIRM1 during the process of monocyte to dendritic cell (DC) differentiation. In line with this observation, HOTAIRM1 RNA expression was downregulated when monocytes differentiated into DCs. Moreover, we found that HOTAIRM1 RNA was regulated by epigenetic factors such as RBBP4 and RBBP7. Mechanistically, we found that the silencing of HOTAIRM1 caused changes in the expression of several monocyte differentiation markers such as CD14 and B7H2. In addition, based on the “competing endogenous RNA” hypothesis, we discovered miR-3960 targeting both HOTAIRM1 and the DC differentiation repression gene, HOXA1, by most possibly constructing a potential competing endogenous RNA network. Increased miR-3960 expression could downregulate both of these two long RNAs and finally lead peripheral blood cells to differentiate into DCs. In summary, our study demonstrates that HOTAIRM1 competitively binds to miR-3960 and finally regulates the process of hematopoiesis, which reveals a novel regulatory mechanism of lncRNA function.

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Epigenetic modification of miR-141 regulates SKA2 by an endogenous ‘sponge’ HOTAIR in glioma

Cited by 62 publications

References 49 publications

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance

MiR‐15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells

Downregulation of long noncoding RNA HOTAIRM1 promotes monocyte/dendritic cell differentiation through competitively binding to endogenous miR-3960

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