LncRNA LINC00689 promotes the growth, metastasis and glycolysis of glioma cells by targeting miR-338-3p/PKM2 axis

Liu, Xin; Zhu, Qiaojuan; Guo, Yang; Xiao, Zunqiang; Hu, Linjun; Xu, Qiuran

doi:10.1016/j.biopha.2019.109069

Cited by 74 publications

(58 citation statements)

References 38 publications

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“…In this study, the expression of miR-338-3p was decreased in glioma, suggesting the potential inhibitory role of this miRNA in glioma, which is supported by previous studies [20]. Moreover, it was reported that miR-338-3p suppressed cell proliferation and metastasis in glioma [21,22]. Similarly, we also confirmed the anticancer role of miR-338-3p in glioma in vitro.…”

Section: Overexpression Of Kcnq1ot1 Up-regulates Rrm2 Expression By Dsupporting

confidence: 90%

“…including bladder cancer, melanoma and oral squamous cell carcinoma [17][18][19]. Moreover, previous research has suggested that dysregulation of miR-338-3p is involved in glioma malignancy [20][21][22], and that Ribonucleotide reductase M2 (RRM2) may contribute to development of glioma [23,24]. More importantly, predictions using starBase 2.0 indicate potential complementary sequences between miR-338-3p and KCNQ1OT1 or RRM2, however sequence interactions between these targets have not been validated previously.…”

Section: Quantitative Real-time Polymerase Chain Reaction (Qrt-pcr) Fmentioning

confidence: 99%

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Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

et al. 2020

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AbstractThe dysregulated lncRNA play essential roles in glioma development. This study aimed to investigate the role and mechanism of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/ antisense transcript 1 (KCNQ1OT1) in glioma progression. Tumor tissues and adjacent normal samples were collected from 30 glioma patients. The expression levels of lncRNA KCNQ1OT1, microRNA (miR)-338-3p and ribonucleotide reductase M2 (RRM2) were detected by quantitative real-time polymerase chain reaction or western blot analyses. Levels of cell viability, apoptosis, cell migration and invasion in glioma cell lines were determined using cell counting kit-8, flow cytometry with annexin V-FITC and trans-well assays, respectively. The role of KCNQ1OT1 in glioma development in vivo was investigated using a xenograft model. The target association between miR-338-3p and KCNQ1OT1 or RRM2 was validated by luciferase reporter assay. The results found that expression of KCNQ1OT1 was enhanced in glioma tissues and cells, and KCNQ1OT1 knockdown inhibited cell viability, migration and invasion, and xenograft tumor growth, but promoted apoptosis. miR-338-3p was targeted via KCNQ1OT1 and could reverse the effect of KCNQ1OT1 on glioma progression. RRM2 was targeted via miR-338-3p and attenuated the suppressive effect of miR-338-3p on glioma cell viability, migration and invasion. Besides, KCNQ1OT1 overexpression increased RRM2 expression, and this event was weakened via miR-338-3p up-regulation. In conclusion, the present finding suggest that silencing of KCNQ1OT1 can suppress the development and progression of glioma by up-regulating miR-338-3p and down-regulating RRM2.

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Section: Overexpression Of Kcnq1ot1 Up-regulates Rrm2 Expression By Dsupporting

confidence: 90%

Section: Quantitative Real-time Polymerase Chain Reaction (Qrt-pcr) Fmentioning

confidence: 99%

Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

et al. 2020

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“…In this study, we found that cell apoptosis induced by circNFIX knockdown might be associated with cell cycle arrest at G0-G1 phase. Moreover, glycolysis is an important way to maintain cell survival in cancers including glioma and lactate is a key product as a biomarker of malignancy [21][22][23]. And HK2 is a key enzyme during glucose metabolism in glycolysis [24].…”

Section: Discussionmentioning

confidence: 99%

CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis

Ding

You

et al. 2019

J Exp Clin Cancer Res

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Background: Circular RNA nuclear factor I X (circNFIX) has been reported to play an important role in glioma progression. However, the mechanism by which circNFIX participates in glioma progression remains poorly understood.Methods: GERIA online were used to analyze the abnormally expressed genes in glioma tissues. The expression levels of circNFIX, microRNA (miR)-378e and Ribophorin-II (RPN2) were measured by quantitative real-time polymerase chain reaction or western blot. Cell cycle distribution, apoptosis, glycolysis, migration and invasion were determined by flow cytometry, special kit and trans-well assays, respectively. The target association between miR-378e and circNFIX or RPN2 was confirmed by luciferase reporter assay, RNA immunoprecipitation and pull-down. Xenograft model was established to investigate the role of circNFIX in vivo.Results: The expression of circNFIX was enhanced in glioma tissues and cells compared with matched controls and high expression of circNFIX indicated poor outcomes of patients. Knockdown of circNFIX led to arrest of cell cycle, inhibition of glycolysis, migration and invasion and promotion of apoptosis in glioma cells. circNFIX was a sponge of miR-378e. miR-378e overexpression suppressed cell cycle process, glycolysis, migration and invasion but promoted apoptosis. miR-378e silence abated the suppressive role of circNFIX knockdown in glioma progression. RPN2 as a target of miR-378e was positively regulated via circNFIX by competitively sponging miR-378e. Silencing circNFIX decreased glioma xenograft tumor growth by regulating miR-378e/RPN2 axis. Conclusion: Knockdown of circNFIX inhibits progression of glioma in vitro and in vivo by increasing miR-378e and decreasing RPN2, providing a novel mechanism for understanding the pathogenesis of glioma.

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“…Generally speaking, lncRNAs are able to be a ceRNA to regulate mRNA expression by competitively combining with miRNAs [25,26]. As for LINC00689, Liu et al explained that LINC00689 might affect glioma progression by regulating miR-338-3p/PKM2 pathways [27]. In current study, LINC00689 was recognized as the upstream of miR-142-3p and worked as a ceRNA to boost USP6NL expression by sequestering miR-142-3p.…”

Section: Discussionmentioning

confidence: 68%

USP6NL mediated by LINC00689/miR-142-3p promotes the development of triple-negative breast cancer

Liu

et al. 2020

BMC Cancer

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Background Triple-negative breast cancer (TNBC), in part because of the high metastasis rate, is one of the most prevalent causes of malignancy-related mortality globally. Ubiquitin specific peptidase 6 N-terminal like (USP6NL) has been unmasked to be implicated in some human cancers. However, the precise biological function of USP6NL in TNBC has not been defined. Methods RNA expression was examined by real-time quantitative PCR (RT-qPCR), while USP6NL protein level was tested through western blot. Besides, cell proliferation was assessed by using colony formation assay, whereas cell apoptosis estimated by flow cytometry analysis, JC-1 assay and TUNEL assay. Transwell assays were adopted to detect the migration and invasion of indicated TNBC cells. Immunofluorescence (IF) assay evaluated epithelial-mesenchymal transitions (EMT) progress in TNBC. Further, RNA immunoprecipitation (RIP), RNA pull down and luciferase reporter assays were implemented for measuring the mutual interplay among USP6NL, miR-142-3p and long intergenic non-protein coding RNA 689 (LINC00689). Results Elevated USP6NL level was uncovered in TNBC cells. RNA interference-mediated knockdown of USP6NL inhibited TNBC cell growth, motility and EMT. Further, USP6NL was proved as the target of a tumor-inhibitor miR-142-3p, and LINC00689 augmented USP6NL expression by absorbing miR-142-3p. Importantly, miR-142-3p deficiency or USP6NL overexpression fully abolished the inhibitory effect of LINC00689 silence on TNBC cellular behaviors. Conclusion All data revealed the important role of USP6NL/LINC00689/miR-142-3p signaling in TNBC. The findings might provide a new and promising therapeutic biomarker for treating patients with TNBC.

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LncRNA LINC00689 promotes the growth, metastasis and glycolysis of glioma cells by targeting miR-338-3p/PKM2 axis

Cited by 74 publications

References 38 publications

Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis

USP6NL mediated by LINC00689/miR-142-3p promotes the development of triple-negative breast cancer

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