Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells

Xiang, Jianping; Guo, Shifeng; Jiang, Shu-Lian; Xu, Yuelong; Li, Jiwei; Li, Li; Xiang, Jinyu

doi:10.3346/jkms.2016.31.5.688

Cited by 49 publications

(33 citation statements)

References 31 publications

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“…Emerging evidence has showed that MALAT1 is implicated in many cancers, including digestive system, gynecological, and urological cancers [12-14]. MALAT1 has also been associated with the clinical outcomes of glioma patients [15], and silencing of MALAT1 leads to the increase of glioma cell apoptosis [16]. It is known that MALAT1 functions as an oncogene partly through inducing EMT.…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA MALAT1 Decreases the Sensitivity of Resistant Glioblastoma Cell Lines to Temozolomide

Li¹,

Yuan²,

Yan³

et al. 2017

Cell Physiol Biochem

102

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Background/Aim: Multidrug resistance (MDR) is largely responsible for the failure of chemotherapy. The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript (MALAT1) has been reported to be closely related to tumor biology. In the present study, whether MALAT1 contributes to the resistance of glioblastoma cell lines to temozolomide (TMZ) was investigated. Methods: The glioblastoma cell lines U251 and U87 were exposed to increasing concentrations of TMZ to generate TMZ-resistant colonies (the U251/TMZ and U87/TMZ cell lines). The expression levels of MALAT1 and proteins related to epithelial-mesenchymal transition (EMT) were detected by real-time PCR and western blot, respectively. After the transfection of si-MALAT1 or pcDNA-MALAT1, cell viability, mRNA expression of MDR-associated proteins (MDR1, MRP5 and LRP1), and protein expression of EMT related proteins (ZEB1, Snail and SLUG) were evaluated. Results: The expression of MALAT1 was upregulated in the U251/TMZ and U87/TMZ cell lines compared to that in U251 and U87 cell lines, respectively. The treatment of si-MALAT1 decreased MDR1, MRP5, and LRP1 expression, enhanced cell sensitivity to TMZ, and downregulated ZEB1 protein expression, whereas pcDNA-MALAT1 had the opposite effects. However, the effects of si-MALAT1 on MDR -associated protein expression, cell viability, and EMT status were reversed by the transfection of pcDNA-ZEB1, and the effects of pcDNA-MALAT1 were reversed by the transfection of si-ZEB1. In vivo, MALAT1 overexpression enhanced tumors’ TMZ resistance and upregulated ZEB1 expression. Conclusion: MALAT1 decreased the sensitivity of resistant glioma cell lines to TMZ by regulating ZEB1.

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Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA MALAT1 Decreases the Sensitivity of Resistant Glioblastoma Cell Lines to Temozolomide

Li¹,

Yuan²,

Yan³

et al. 2017

Cell Physiol Biochem

102

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“…A universal siRNA with no homology with mammalian gene sequence was used as negative control. Sequences were designed as follows: MALAT1, forward 5'-GGG CUU CUC UUA ACA UUU AUU-3', reverse 5'-UAA AUG UUA AGA GAA GCC CUU)-3' (50 nM) (27,28); SOX2OT, forward 5'-GGA GAU UGU GAC CUG GCU UTT-3', reverse 5'-AAG CCA GGU CAC AAU CUC CTT)-3' (50 nM) (29); ANRIL, forward 5'-GGU CAU CUC AUU GCU CUA UTT-3', reverse 5'-CCA GUA GAG UAA CGA GAU ATT)-3' (25 nM) (24,30); and universal siRNA negative control, forward 5'-UUC UCC GAA CGU GUC ACG UTT-3' and reverse 5'-ACG UGA CAC GUU CGG AGA ATT-3' (50 nM). Transfections were performed using Lipofectamine ® 2000 (Invitrogen; Thermo Fisher Scientific, Inc.) at room temperature for 25 min and at 37˚C in an incubator containing 5% CO 2 for 6 h. Plasmids were constructed and extracted in our laboratory and siRNAs were synthesized by Shanghai GenePharma Co., Ltd. (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

lncRNAs combine and crosstalk with NSPc1 in ATRA‑induced differentiation of U87 glioma cells

Liang

Wang

et al. 2019

Oncol Lett

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Nervous system polycomb 1 (NSPc1) is a member of the polycomb group (PcG) family of proteins and has been demonstrated to maintain the differentiation and pluripotency of stem cells. Long non-coding RNAs (lncRNAs) have been demonstrated to be involved in the control of pluripotency and differentiation in embryonic and pluripotent cells. In the present study, the expression levels of NSPc1 were associated with the malignant potential of various glioma cell lines. Additionally, lncRNAs were differentially expressed in glioblastoma cell lines. Following induced differentiation of U87 glioblastoma cells with all-trans retinoic acid, the expression levels of NSPc1 decreased initially, reaching its lowest point on day 6, but then subsequently increased until day 10. The expression of lncRNA candidates decreased in the cell differentiation stage. Additionally, the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), sex-determining region of the Y chromosome-box 2 overlapping transcript (SOX2OT) and antisense non-coding RNA in the INK4 locus (ANRIL) was significantly altered relative to the expression levels of NSPc1. RNA immunoprecipitation (RIP) assays demonstrated that MALAT1, SOX2OT and ANRIL bind to NSPc1 in U87 glioblastoma cells and the enrichment of ANRIL in anti-NSPc1 antibody group was associated with the expression levels of NSPc1 during U87 cell differentiation. Small interfering RNA mediated downregulation of NSPc1 expression with MALAT1, SOX2OT and ANRIL, inhibited the proliferation, and promoted apoptosis in U87 cells. The results of the present study demonstrate that MALAT1, SOX2OT and ANRIL combine and crosstalk with NSPc1 in U87 cells to affect proliferation and apoptosis.

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“…As NEAT2 (nuclear-enriched abundant transcript 2), also known as MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), is a highly conserved lncRNA associated with the metastatic potential of tumor cells, Han et al (2016a) found that the knockdown of NEAT2 by RNA interference could promote the invasion and proliferation of glioma cells. Concomitantly, the apoptosis rate of the glioma cell lines is shown to dramatically increase ( Han et al, 2016a ; Xiang et al, 2016 ). Over all, these results indicate that an investigation into the abnormal expression profiles of lncRNAs may help in the understanding of oncogenesis and identify novel potential treatment targets in glioma research and therapy.…”

Section: Profile Of Lncrnas In Human Glioma Research and Therapymentioning

confidence: 99%

An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas

Yan

et al. 2017

Front. Mol. Neurosci.

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Long non-coding RNAs (LncRNAs) are essential epigenetic regulators with critical roles in tumor initiation and malignant progression. However, the roles and mechanisms of aberrantly expressed lncRNAs in the pathogenesis of gliomas are not fully understood. With the development of deep sequencing analyses, an extensive amount of functional non-coding RNAs has been discovered in glioma tissues and cell lines. Additionally, the contributions of several lncRNAs, such as Hox transcript antisense intergenic RNA, H19 and Colorectal neoplasia differentially expressed, previously reported to be involved in other pathogenesis and processes to the oncogenesis of glioblastoma are currently addressed. Thus, lncRNAs detected in tumor tissues could serve as candidate diagnostic biomarkers and therapeutic targets for gliomas. To understand the potential function of lncRNAs in gliomas, in this review, we briefly describe the profile of lncRNAs in human glioma research and therapy. Then, we discuss the individual lncRNA that has been under intensive investigation in glioma research, and the focus is its mechanism and clinical implication.

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Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells

Cited by 49 publications

References 31 publications

Long Non-Coding RNA MALAT1 Decreases the Sensitivity of Resistant Glioblastoma Cell Lines to Temozolomide

Long Non-Coding RNA MALAT1 Decreases the Sensitivity of Resistant Glioblastoma Cell Lines to Temozolomide

lncRNAs combine and crosstalk with NSPc1 in ATRA‑induced differentiation of U87 glioma cells

An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas

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