LncRNA HOXA-AS2 promotes glioblastoma carcinogenesis by targeting miR-885-5p/RBBP4 axis

Shou, Jixin; Gao, Haidong; Cheng, Sen; Wang, Bingbing; Guan, Haibo

doi:10.1186/s12935-020-01690-1

Cited by 23 publications

(18 citation statements)

References 35 publications

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“…Recent research emphasizes that epigenomic factors play a crucial role in the development of PD, and it is assumed that the initiation of PD is promoted by a combination of a genetic predisposition and environmental triggers [ 35 , 36 ]. Although several studies have demonstrated that HOXA-AS2 promotes tumor proliferation by serving as an “miRNA sponge” [ 30 , 37 , 38 ], it has also been shown to enhance gastric cancer proliferation by epigenetically silencing the expression of p21, plk3, and DDIT3 [ 39 , 40 ]. A study highlighted the role of aberrant DNA methylation of the HOXA gene cluster in the pathogenesis of Alzheimer’s disease [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOXA-AS2 regulates microglial polarization via recruitment of PRC2 and epigenetic modification of PGC-1α expression

Yang

Zhang

Chen

et al. 2021

J Neuroinflammation

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Background Microglia-mediated neuroinflammation plays an important role in Parkinson’s disease (PD), and it exerts proinflammatory or anti-inflammatory effects depending on the M1/M2 polarization phenotype. Hence, promoting microglia toward the anti-inflammatory M2 phenotype is a potential therapeutic approach for PD. Long noncoding RNAs (lncRNAs) are crucial in the progression of neurodegenerative diseases, but little is known about their role in microglial polarization in PD. Methods In our study, we profiled the expression of lncRNAs in the peripheral blood mononuclear cells (PBMCs) of PD patients using a microarray. RT-qPCR was used to evaluate the lncRNA levels and mRNA levels of cytokines and microglial cell markers both in vitro and in vivo. RIP and ChIP assays were analyzed for the underlying mechanism of lncRNA regulating microglial polarization. Results We found that HOXA-AS2 was upregulated in the PBMCs of PD patients and negatively associated with peroxisome proliferator-activated receptor gamma coactivator-1a (PGC-1α) expression. Moreover, HOXA-AS2 knockdown significantly repressed microglial M1 polarization and promoted M2 polarization by regulating PGC-1α expression. Mechanistic investigations demonstrated that HOXA-AS2 could directly interact with polycomb repressive complex 2 (PRC2) and modulate the histone methylation of the promoter of PGC-1α. Conclusions Our findings identify the upregulated lncRNA HOXA-AS2 promotes neuroinflammation by regulating microglial polarization through interacts with the PRC2 complex and epigenetically silencing PGC-1α. HOXA-AS2 may be a potential therapeutic target for microglia-mediated neuroinflammation in patients with PD.

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Section: Discussionmentioning

confidence: 99%

LncRNA HOXA-AS2 regulates microglial polarization via recruitment of PRC2 and epigenetic modification of PGC-1α expression

Yang

Zhang

Chen

et al. 2021

J Neuroinflammation

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“…Then, the BrdU Cell Proliferation Assay Kit (Cat#: 6813, CST, MA, USA) was used to detect cell proliferation. BrdU (10 μM) was added to the plate and incubated for 4 h and then incubated with secondary antibody for another 1 h. The OD value was examined using a multimode plate reader at a wavelength of 450 nm [ 17 ].…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

Shi

et al. 2021

Bioengineered

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As the most common and aggressive malignant form of skin cancer, melanoma has a poor prognosis in its late stage. MicroRNA (miR)-520d-3p has been reported as a key modulator that regulates the development of different types of cancer, but its role in melanoma remains unclear. The purpose of this study was to investigate the role and mechanism of miR-520d-3p in melanoma. The expression of anti-silencing function 1B histone chaperone ( ASF1B ) and miR-520d-3p in melanoma tissues and cells was detected by reverse transcription-quantitative polymerase chain reaction. The interaction between ASF1B and miR-520d-3p was verified by luciferase activity detection. Cell counting kit-8, bromodeoxyuridine, fluorescein isothiocyanate, and cell adhesion assays were performed to detect cell viability, proliferation, apoptosis, and adhesion in melanoma cells. ASF1B expression was evidently increased, whereas miR-520d-3p level was downregulated in melanoma tissues and cells. Overexpression of ASF1B enhanced cell growth and adhesion and hampered cell apoptosis in melanoma cells. Furthermore, miR-520d-3p suppressed the tumorigenic effects of melanoma cells. Moreover, miR-520d-3p suppressed the expression of ASF1B to suppress melanoma tumorigenesis. In conclusion, we have found out that miR-520d-3p suppressed melanoma tumorigenesis by inhibiting ASF1B , which could be a promising target for melanoma therapy.

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“…Liao et al demonstrated that lncRNA MALAT1 facilitates the malignancy of GBM via the miR-199a/ZHX1 axis [ 14 ]. Shou et al revealed that lncRNA HOXA-AS2 is upregulated in GBM and promotes cancer development via regulating the miR-885-5p/RBBP4 axis [ 15 ]. MiR-34a expression is downregulated in GBM tissues and inhibits GBM progression [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 Antisense RNA 1

Jin

Long

et al. 2022

Bioengineered

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MicroRNA-1269 (miR-1296) promotes esophageal cancer. However, its role in other cancers, such as glioblastoma (GBM) is unclear. We predicted that miR-1269 might interact with long non-coding RNA (lncRNA) SLC16A1 Antisense RNA 1 (SLC16A1-AS1), a critical player in GBM. We then studied the interaction between SLC16A1-AS1 and miR-1269 in GBM. In this study, paired GBM and non-tumor tissues were used to analyze the expression of SLC16A1-AS1 and premature and mature miR-1269. The interaction of SLC16A1-AS1 with premature miR-1269 was analyzed with RNA pull-down assay and dual-luciferase reporter assay. Cellular fractionation assay was applied to determine the subcellular location of SLC16A1-AS1. Overexpression assays were applied to determine the role of SLC16A1-AS1 in miR-1269 maturation. BrdU, Transwell and cell apoptosis assays were performed to analyze the role of SLC16A1-AS1 and miR-1269 in GBM cell proliferation, migration, and invasion. Interestingly, we observed the upregulation of premature miR-1269 and downregulation of mature miR-1269 in GBM. SLC16A1-AS1 was also overexpressed in GBM. The direct interaction of SLC16A1-AS1 with premature miR-1269 was observed. SLC16A1-AS1 suppressed miR-1269 maturation and promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while miR-1269 displayed the opposite trend. SLC16A1-AS1 partly reversed the effects of miR-1269 on GBM cell proliferation, movement and apoptosis. Moreover, SLC16A1-AS1 overexpression increased the level of ki-67, CDK4 and Bcl-2 in LN-229 and LN-18 cells. However, miR-1269 could partly reverse the effect of SLC16A-AS1 on protein levels. Overall, miR-1269 is downregulated in GBM and its maturation is regulated by SLC16A1-AS1.

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LncRNA HOXA-AS2 promotes glioblastoma carcinogenesis by targeting miR-885-5p/RBBP4 axis

Cited by 23 publications

References 35 publications

LncRNA HOXA-AS2 regulates microglial polarization via recruitment of PRC2 and epigenetic modification of PGC-1α expression

LncRNA HOXA-AS2 regulates microglial polarization via recruitment of PRC2 and epigenetic modification of PGC-1α expression

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 Antisense RNA 1

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