The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma

Wang, Qiang; Teng, Yiwan; Wang, Rong; Deng, Danni; You, Yijie; Peng, Ya; Shao, Nan; Zhi, Feng

doi:10.18632/oncotarget.23960

Cited by 40 publications

(38 citation statements)

References 55 publications

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“…34 The long noncoding RNA SNHG14 represses cell proliferation but boosts cell apoptosis of glioma cells by sponging miR-92a-3p. 35 MAGI2-AS3 has been reported as an anti-tumor lncRNA in several cancers, including hepatocellular cancer and breast cancer. 15,26 The downregulation of MAGI2-AS3 has been proved in NSCLC including LUAD and LUSC.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis</p>

He¹,

Zhou²,

Li³

et al. 2020

CMAR

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Background: Lung squamous cell carcinoma (LUSC) accounts for approximately 30% of all lung cancers that possesses the highest occurrence and mortality in all cancer types. Long noncoding RNAs have been reported to modulate tumor development for several decades. Aim of the Study: This research aims to investigate the role of MAGI2-AS3 in LUSC. Methods: RT-qPCR tested genes (including MAGI2-AS3, miR-374a/b-5p and CADM2) expression. Cell proliferation was detected by colony formation and EdU assays. Cell migration and invasion were evaluated by transwell assay. Flow cytometry analysis of apoptotic cells and Western blot analysis on apoptosis-related genes were applied to measure cell apoptosis. Nuclear-cytoplasmic fractionation and FISH assay positioned MAGI2-AS3. The combination between miR-374a/b-5p and MAGI2-AS3 (or CADM2) was determined by luciferase reporter assay and RIP assay. Results: MAGI2-AS3 inhibited the proliferative, migratory and invasive capability of LUSC cells with upregulated expression. Additionally, MAGI2-AS3 overexpression promoted cell apoptosis. We discovered that MAGI2-AS3 was located in the cytoplasm. Hereafter, we found out that MAGI2-AS3 targeted miR-374a/b-5p. CADM2 was targeted by miR-374a/ b-5p. Finally, rescue assays indicated that the promoting effects of miR-374a/b-5p amplification on biological activities were restored by CADM2 addition. Conclusion: In conclusion, lncRNA MAGI2-AS3 suppressed LUSC by regulating miR-374a/b-5p/CADM2 axis, which might potentially serve as a therapeutic marker for LUSC patients.

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Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis</p>

He¹,

Zhou²,

Li³

et al. 2020

CMAR

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“…Previous studies have demonstrated that miR-92a-3p is involved in many different types of diseases such as T-cell acute lymphoblastic leukemia [32], renal injury-associated atherosclerosis [33] and colorectal cancer [34]. However, Wang et al [35] indicated that miR-92a-3p could reverse the anti-tumor abilities of small nucleolar RNA host gene 14 (SNHG14) in the progression of glioma. In this experiment, the mice were treated intrathecally by agomiR-92 to investigate the functions of miR-92a-3p, and the data demonstrated that the up-regulation of miR-92a-3p observably promoted the functional recovery of the mice after SCI surgery, meanwhile, the cell apoptosis of spinal cord tissues of SCI mice was also obviously suppressed by the treatment of agomiR-92.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog

Wang

et al. 2020

Bioscience Reports

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Spinal cord injury (SCI) is a neurological disease commonly caused by traumatic events on spinal cords. MiRNA-92a-3p is reported to be down-regulated after SCI. Our study investigated the effects of up-regulated miR-92a-3p on SCI and the underlying mechanisms. SCI mice model was established to evaluate the functional recovery of hindlimbs of mice through open-field locomotion and scored by Basso, Beattie, and Bresnahan (BBB) locomotion scale. Apoptosis of spinal cord cells was determined by flow cytometry. The effects of miR-92a-3p on SCI were detected by intrathecally injecting miR-92a-3p agomiR (agomiR-92) into the mice prior to the establishment of SCI. Phosphatase and tensin homolog (PTEN) was predicted as a target of miR-29a-3p by TargetScan. We further assessed the effects of agomiR-92 or/and overexpressed PTEN on apoptosis rates and apoptotic protein expressions in SCI mice. Moreover, the activation of protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling was determined by Western blot. The results showed that compared with the sham-operated mice, SCI mice had much lower BBB scores, and theapoptosis rate of spinal cord cells was significantly increased. After SCI, the expression of miR-92a-3p was down-regulated, and increased expression of miR-92a-3p induced by agomiR-92 further significantly increased the BBB score and decreased apoptosis. PTEN was specifically targeted by miR-92a-3p. In addition, the phosphorylation levels of Akt and mTOR were up-regulated under the treatment of agomiR-92. Our data demonstrated that the neuroprotective effects of miR-92a-3p on spinal cord safter SCI were highly associated with the activation of the PTEN/AKT/mTOR pathway.

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“…15 Recently, Liu et al 16 demonstrated that SNHG14 could act as a ceRNA to promote initiation and progression of clear cell renal cell carcinoma by regulating N-WASP protein. Another report from Wang et als 17 showed that SNHG14 is a tumour suppressor gene by inhibiting proliferation and invasion in glioma. These contradictory conclusions lead us to identify the function of SNHG14 in breast cancer.…”

mentioning

confidence: 99%

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

Huang

Wang

et al. 2018

J Cellular Molecular Medi

101

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Currently, resistance to trastuzumab, a human epidermal growth factor receptor 2 (HER2) inhibitor, has become one major obstacle for improving the clinical outcome of patients with advanced HER2+ breast cancer. While cell behaviour can be modulated by long non‐coding RNAs (lncRNAs), the contributions of lncRNAs in progression and trastuzumab resistance of breast cancer are largely unknown. To this end, the involvement and regulatory functions of lncRNA SNHG14 in human breast cancer were investigated. RT‐qPCR assay showed that SNHG14 was up‐regulated in breast cancer tissues and associated with trastuzumab response. Gain‐ and loss‐of‐function experiments revealed that overexpression of SNHG14 promotes cell proliferation, invasion and trastuzumab resistance, whereas knockdown of SNHG14 showed an opposite effect. PABPC1 gene was identified as a downstream target of SNHG14, and PABPC1 mediates the SNHG14‐induced oncogenic effects. More importantly, ChIP assays demonstrated that lncRNA SNHG14 may induce PABPC1 expression through modulating H3K27 acetylation in the promoter of PABPC1 gene, thus resulting in the activation of Nrf2 signalling pathway. These data suggest that lncRNA SNHG14 promotes breast cancer tumorigenesis and trastuzumab resistance through regulating PABPC1 expression through H3K27 acetylation. Therefore, SNHG14 may serve as a novel diagnostic and therapeutic target for breast cancer patients.

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The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma

Cited by 40 publications

References 55 publications

<p>Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis</p>

<p>Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis</p>

MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

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