LncRNA <i>TUG1</i> promotes the progression of colorectal cancer via the miR-138-5p/ZEB2 axis

Yan, Zhaowei; Bi, Miaomiao; Zhang, Qiyu; Song, Yumei; Hong, Sen

doi:10.1042/bsr20201025

Cited by 27 publications

(21 citation statements)

References 28 publications

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“…21 A series of lncRNAs regulated colorectal cancer progression in this way, such as TUG1, ZFAS1 and LOC101927746. [22][23][24] In order to investigate the mechanism of EWSA1-regulated CRC progression, we wanted to know whether lncRNA-miRNA-mRNA ceRNA network was involved. In the present study, we predicted miR-326 as the target of EWSAT1 with the help of bioinformatics methods.…”

Section: Discussionmentioning

confidence: 99%

LncRNA EWSAT1 Promotes Colorectal Cancer Progression Through Sponging miR-326 to Modulate FBXL20 Expression

Liu¹,

Huang²,

Liao³

et al. 2021

OTT

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Background: Ewing sarcoma-associated transcript 1 (EWSAT1) has been reported to be a pivotal modulator in a series of cancers. However, the function of EWSAT1 in colorectal cancer (CRC) has not been elaborated. This study aimed to explore the role of EWSAT1 in CRC progression and the underlying mechanisms. Methods: The expression patterns of EWSAT1, miR-326 and FBXL20 were examined by qCRCR. Si-EWSAT1 was transfected to study the effects of EWSAT1 on cell proliferation and metastasis. Rescue experiments were performed to investigate the underlying mechanisms in vitro. Xenograft models were used to evaluate the role of EWSAT1 in vivo. Results: We found that EWSAT1 was highly expressed in CRC tissues and cell lines and associated with poor overall survival. In vitro, knockdown of EWSAT1 suppressed the cell proliferation, migration and invasion. Moreover, miR-326 was found to be a target of EWSAT1, and miR-326 inhibitor could partially reverse the effects on CRC cell progression induced by si-EWSAT1. Subsequently, we validated FBXL20 as a vital downstream target for miR-326, and EWSAT1 positively regulated FBXL20 via miR-326 in vitro. In addition, these findings were confirmed by in vivo experiments. Conclusion:Taken together, the data showed that EWSAT1 promoted CRC progression via targeting miR-326/FBXL20 pathway, which might provide a novel therapeutic target for CRC treatment.

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Section: Discussionmentioning

confidence: 99%

LncRNA EWSAT1 Promotes Colorectal Cancer Progression Through Sponging miR-326 to Modulate FBXL20 Expression

Liu¹,

Huang²,

Liao³

et al. 2021

OTT

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“…LncRNA TUG1 is expressed in the retina and brain and was discovered to serve an important role in numerous cancer types, including colorectal, esophageal and bladder cancer (43)(44)(45). However, to the best of our knowledge, the underlying mechanism of action of TUG1 in age-related cataracts remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA TUG1 protects lens epithelial cells from oxidative stress‑induced injury by regulating miR‑196a‑5p expression in age‑related cataracts

Shen

Zhou

2021

Exp Ther Med

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Oxidative stress plays an important role in the pathogenesis of cataracts. Under oxidative stress, apoptosis of lens epithelial cells (LECs) is activated, which may cause lens opacity and accelerate the development of cataracts. Long non-coding RNA (lncRNA) and microRNA (miRNA/miR) are involved in cataracts. Previous studies have demonstrated that lncRNA taurine upregulated 1 (TUG1) promotes cell apoptosis induced by ultraviolet radiation by downregulating the expression of miR-421. However, the mechanism underlying TUG1 in age-related cataract remains to be elucidated. The present study aimed to investigate the effect of TUG1 in age-related cataracts and to determine the related underlying molecular mechanism. In the present study, the association between TUG1 and microRNA (miR)-196a-5p was predicted using StarBase and verified using a dual luciferase reporter assay in 293 cells. The LEC line SRA01/04 was exposed to 200 µM hydrogen peroxide (H 2 O 2 ) for 24 h to establish an in vitro oxidative stress model. The mRNA expression levels of TUG1 and miR-196a-5p were analyzed using reverse transcription-quantitative PCR, whilst cell viability and apoptosis were determined using MTT and flow cytometry assays, respectively. The protein expression levels of cleaved caspase-3 and caspase-3 in SRA01/04 cells were determined using western blotting. The results of the present study revealed that TUG1 directly targeted miR-196a-5p expression. In addition, the expression levels of miR-196a-5p were downregulated in SRA01/04 cells following oxidative stress, whilst TUG1 expression was upregulated. Cell transfection with TUG1-small interfering RNA (siRNA) upregulated miR-196a-5p expression levels in SRA01/04 cells, which was reversed following co-transfection with the miR-196a-5p inhibitor. Transfection with TUG1-siRNA also reduced the levels of H 2 O 2 -induced oxidative damage in SRA01/04 cells, which was demonstrated by increased cell viability, reduced levels of apoptosis and downregulated cleaved caspase-3 levels. Conversely, transfection with the miR-196a-5p inhibitor reversed these effects aforementioned. Overexpression of miR-196a-5p reduced H 2 O 2 -induced oxidative damage in SRA01/04 cells. In conclusion, findings from the present study suggested that knocking down TUG1 expression may protect LECs from oxidative stress-induced apoptosis by upregulating the expression of miR-196a-5p.

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“…(15) Although taurine has a number of anticancer and anti-inflammatory effects [193], its induction of the lncRNA, taurine upregulated (TUG)1, leads to increased tumour proliferation, metastasis and survival [194]. TUG-1 also induces ACC, thereby lowering acetyl-CoA and inhibits miR-138 [195], and therefore the miR-138 inhibition of PD-1. TUG-1 also binds to the PGC-1α promotor, inhibiting PGC-1α induction of optimal mitochondrial function [196], indicating that it will have significant effects on metabolism and miRNA patterning.…”

Section: Future Researchmentioning

confidence: 99%

Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types—Tumour Microenvironment and Metabolism

Anderson¹

2020

IJMS

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This article reviews the dynamic interactions of the tumour microenvironment, highlighting the roles of acetyl-CoA and melatonergic pathway regulation in determining the interactions between oxidative phosphorylation (OXPHOS) and glycolysis across the array of cells forming the tumour microenvironment. Many of the factors associated with tumour progression and immune resistance, such as yin yang (YY)1 and glycogen synthase kinase (GSK)3β, regulate acetyl-CoA and the melatonergic pathway, thereby having significant impacts on the dynamic interactions of the different types of cells present in the tumour microenvironment. The association of the aryl hydrocarbon receptor (AhR) with immune suppression in the tumour microenvironment may be mediated by the AhR-induced cytochrome P450 (CYP)1b1-driven ‘backward’ conversion of melatonin to its immediate precursor N-acetylserotonin (NAS). NAS within tumours and released from tumour microenvironment cells activates the brain-derived neurotrophic factor (BDNF) receptor, TrkB, thereby increasing the survival and proliferation of cancer stem-like cells. Acetyl-CoA is a crucial co-substrate for initiation of the melatonergic pathway, as well as co-ordinating the interactions of OXPHOS and glycolysis in all cells of the tumour microenvironment. This provides a model of the tumour microenvironment that emphasises the roles of acetyl-CoA and the melatonergic pathway in shaping the dynamic intercellular metabolic interactions of the various cells within the tumour microenvironment. The potentiation of YY1 and GSK3β by O-GlcNAcylation will drive changes in metabolism in tumours and tumour microenvironment cells in association with their regulation of the melatonergic pathway. The emphasis on metabolic interactions across cell types in the tumour microenvironment provides novel future research and treatment directions.

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LncRNA TUG1 promotes the progression of colorectal cancer via the miR-138-5p/ZEB2 axis

Cited by 27 publications

References 28 publications

LncRNA EWSAT1 Promotes Colorectal Cancer Progression Through Sponging miR-326 to Modulate FBXL20 Expression

LncRNA EWSAT1 Promotes Colorectal Cancer Progression Through Sponging miR-326 to Modulate FBXL20 Expression

Knockdown of lncRNA TUG1 protects lens epithelial cells from oxidative stress‑induced injury by regulating miR‑196a‑5p expression in age‑related cataracts

Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types—Tumour Microenvironment and Metabolism

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