Knockdown of long non‐coding RNA XIST suppresses nasopharyngeal carcinoma progression by activating miR‐491‐5p

Cheng, Qiang; Xu, Xiaoxing; Jiang, Hui; Xu, Lina; Li, Qiang

doi:10.1002/jcb.26535

Cited by 28 publications

(16 citation statements)

References 25 publications

(57 reference statements)

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“…In our study, targeting XIST significantly reduced cell viability and increased cell apoptosis in vitro in U2OS cells, and targeting XIST suppressed tumorigenesis in vivo. Our findings are similar to those of the recent reports [31,32] and contrary to the results of recent reports [33,34]. However, the underlying mechanism by which XIST mediates gene expression and participates in tumorigenesis remains to be clarified.…”

Section: Discussionsupporting

confidence: 86%

“…In bladder cancer cells in vitro, targeting XIST suppressed cell invasion and proliferation by downregulation of p53 [30]. In nasopharyngeal carcinoma (NPC), targeting XIST inhibited NPC cell proliferation and invasion in vitro and NPC tumor growth in vivo [31]. Further investigation revealed that XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression [32].…”

Section: Discussionmentioning

confidence: 99%

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Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Gao

Chen

et al. 2019

Bioengineered

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The long noncoding RNA X-inactive specific transcript (XIST) plays vital roles in tumor progression. However, the underlying mechanisms remain unclear. This study investigated the effects and mechanisms of targeting XIST on osteosarcoma (OS) cells in vitro and in vivo. We used shRNA to knockdown XIST to evaluate cell growth and apoptosis in U2OS cells in vitro and xenograft formation in vivo. An observed relationship between XIST and the p53 upregulated modulator of apoptosis (PUMA) and nuclear factor-kappa B (NF-kB) pathway was further explored by using small interfering RNA (siRNA). Our results showed that suppression of XIST by short hairpin RNA (shRNA) impeded U2OS cell growth, induced apoptosis and lessened OS xenograft tumor growth. Targeting XIST increased NF-kB-dependent PUMA upregulation in U2OS cells. Upregulation of PUMA is correlated with suppression of XIST-induced apoptosis in U2OS cells. Therefore, inhibition of XIST could promote U2OS cell death via activation of NF-kB/PUMA pathways.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Gao

Chen

et al. 2019

Bioengineered

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“…miR-491-5p was a tumor suppressor in several cancer types [ 20 – 23 ]. Aberrant expression of miR-491-5p was the consequence of upregulated circRNA circ_0001361 and lncRNA XIST in bladder cancer and nasopharyngeal carcinoma respectively [ 24 , 25 ]. In glioma, miR-491-5p was decreased in cancer tissues and correlated with good prognosis [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA LBX2-AS1 enhances glioma proliferation through downregulating microRNA-491-5p

et al. 2020

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Background: Dysregulation of lncRNAs is frequent in glioma and has emerged as an important mechanism involved in tumorigenesis. Previous analysis of Chinese Glioma Genome Atlas (CGGA) database indicated that LBX2-AS1 expression is one of differentially expression lncRNA between lower grade glioma (LGG) (grade II and III) and glioblastoma multiforme (GBM). However, the function and mechanism of LBX2-AS1 in glioma has not been evaluated yet. Methods: Here, we analyzed the expression of LBX2-AS1 in GTEx data (normal brain), TCGA-LGG and TCGA-GBM. RT-PCR was performed to detect LBX2-AS1 in surgery obtained normal brain and glioma. CCK-8 kit and Annexin V-FITC-PI Apoptosis Detection Kit were used to study the function of LBX2-AS1 on glioma proliferation and apoptosis. Bioinformatic analysis, RNA immunoprecipitation, RT-PCR, western blotting and dual luciferase reporter assay were carried out to investigate the target miRNA of LBX2-AS1. The discovered mechanism was validated by the rescue assay. Results: Following study of GTEx and TCGA data, LBX2-AS1 was significantly elevated in glioma compared with normal brain and in GBM compared with LGG. Higher expression of LBX2-AS1 was associated with poor prognosis of patients with glioma. Expression of LBX2-AS1 was positively correlated with pathology classification of glioma. Knockdown of LBX2-AS1 inhibited cell proliferation and induced cell apoptosis in glioma. LBX2-AS1 have complimentary binding site for tumor suppressor miR-491-5p and we showed that LBX2-AS1 sponged miR-491-5p to upregulate TRIM28 expression in glioma cells. TRIM28 overexpression attenuated the effect of LBX2-AS1 knockdown on glioma cells. Conclusions: In conclusion, LBX2-AS1 was an increased lncRNA in glioma. Mechanistically, LBX2-AS1 promoted glioma cell proliferation and resistance to cell apoptosis via sponging miR-491-5p.

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“…23 Knockdown of lncRNA XIST suppresses NPC progression by activating miR-491-5p. 24 SOX2-OT has been reported to be upregulated in laryngeal squamous cell carcinoma and regulate osteosarcoma cells proliferation and motility through modulating SOX2. 9,25 Nevertheless, the biological significance and regulatory mechanism of SOX2-OT in NPC progression are largely to be clarified.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SOX2‐OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR‐146b‐5p/HNRNPA2B1 pathway

Enqin¹,

2019

J of Cellular Biochemistry

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Nasopharyngeal carcinoma (NPC) is an aggressive malignancy with a high mortality on account of its frequent metastasis and poor prognosis. An extensive body of investigations has proven that long noncoding RNAs are implicated in a variety of biological processes. Although SOX2‐OT has been reported to play an oncogenic role in osteosarcoma, the mechanism of SOX2‐OT‐driven NPC progression is still obscure. The aim of this study was to elucidate the biological function of SOX2‐OT and the related possible mechanism in NPC. In our study, SOX2‐OT was notably elevated in NPC samples and cells. Further, a high expression level of SOX2‐OT was correlated with poor clinical outcomes of NPC. Results from loss‐of‐function experiments suggested that knockdown of SOX2‐OT repressed cell proliferation, arrested cell cycle, facilitated cell apoptosis, and inhibited cell metastasis of NPC. To further investigate the molecular mechanism of SOX2‐OT, miR‐146b‐5p was found to directly bind to SOX2‐OT, which mediated the role of SOX2‐OT in NPC tumorigenesis. In addition, HNRNPA2B1 was a target of miR‐146b‐5p and SOX2‐OT modulated the expression of HNRNPA2B1 through competitively binding to miR‐146b‐5p. At last, we discovered that SOX2‐OT regulated NPC progression by targeting miR‐146b‐5p/HNRNPA2B1 pathway, which may provide more innovative targets for the treatment of patients with NPC.

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Knockdown of long non‐coding RNA XIST suppresses nasopharyngeal carcinoma progression by activating miR‐491‐5p

Cited by 28 publications

References 25 publications

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

RETRACTED ARTICLE: Long non-coding RNA LBX2-AS1 enhances glioma proliferation through downregulating microRNA-491-5p

LncRNA SOX2‐OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR‐146b‐5p/HNRNPA2B1 pathway

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