Knockdown of TUG1 by shRNA inhibited renal cell carcinoma formation by miR-299–3p/VEGF axis in vitro and in vivo

Li, Yunsheng; Zheng, Duo; Pan, Liutong; Dai, Yuanting; Shasha, Cai; Zhao, Leilei; Zhu, Huiping

doi:10.1016/j.ejphar.2019.172536

Cited by 21 publications

(14 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LncRNA plays a pivotal part in carcinogenesis and tumor progression. One study has uncovered that knockdown of TUG1 via shRNA can inhibit the formation of renal cell carcinoma in vivo and in vitro through the miR-299-3p/VEGF axis [18], and one other study by Yang et al [19] has revealed that lncRNA TUG1 participates in pulmonary vascular remodeling of hypoxic pulmonary hypertension mice through miR-374c-mediated Foxc1. Our study was to explore the effect of lncRNA TUG1 on the progression and biological function of CRC by regulating the miR-138-5p/ZEB2 axis.…”

Section: Discussionmentioning

confidence: 99%

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

Yan

Zhang³

et al. 2020

Bioscience Reports

View full text Add to dashboard Cite

To explore the role of long-chain non-coding RNA (lncRNA) taurine up-regulated gene 1 (TUG1) in the development of colorectal cancer (CRC) via the miR-138-5p/zinc finger E-box-binding homeobox 2 (ZEB2) axis. Eighty-four CRC tissue specimens and 84 corresponding paracancerous tissue specimens were sampled from 84 patients with CRC admitted to the First Hospital of Jilin University from January 2018 to September 2019. The TUG1 expression in the specimens was determined, and its value in diagnosis and prognosis of CRC was analyzed. Additionally, constructed stable and transient overexpresison vectors and inhibition vectors were transfected into CRC cells. The MTT, transwell, and flow cytometry were adopted for analysis on the proliferation, invasion, and apoptosis of transfected cells, respectively, and a dual luciferase reporter (DLR) assay was carried out for correlation determination between TUG1 and miR-138-5p and between miR-138-5p and ZEB2. TUG1 was up-regulated in CRC, and serum TUG1 could be adopted as a diagnostic marker of CRC, with area-under-the-curve (AUC) larger than 0.8. In addition, siRNA-TUG1, shRNA-TUG1, miR-138-5p-mimics, and miR-138-5p-inhibitor were transfected into cells, and it turned out that overexpressing miR-138-5p and inhibiting ZEB2 exerted the same effects. The DLR assay revealed that TUG1 was able to targetedly regulate miR-138-5p, and miR-138-5p could targetedly regulate ZEB2, and in vitro experiments revealed that TUG1 could affect the epithelial-to-mesenchymal transition (EMT) of CRC via the miR-138-5p/ZEB2 axis. TUG1 could promote the development of CRC via the miR-138-5p/ZEB2 axis.

show abstract

Section: Discussionmentioning

confidence: 99%

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

Yan

Zhang³

et al. 2020

Bioscience Reports

View full text Add to dashboard Cite

show abstract

“…As a new lncRNA that has just been discovered, TUG1 has been recognized as an oncogene in most cancers to involve in the regulation of cancer progression [26,27]. However, there are few studies on the molecular regulation mechanism of TUG1 on HCC.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

View full text Add to dashboard Cite

Background: Accumulating evidence indicates that the long noncoding RNA taurine upregulated gene 1(TUG1) plays a critical role in cancer progression and metastasis. However, the overall biological role and clinical significance of TUG1 in hepatocellular carcinoma (HCC) remain largely unknown. Methods:The expressions of TUG1, microRNA-216b-5p and distal-less homeobox 2 (DLX2) were detected by Quantitative real-time polymerase chain reaction (qRT-PCR). The target relationships were predicted by StarBase v.2.0 or TargetScan and confirmed by dual-luciferase reporter assay. The cell growth, apoptosis, migration and invasion were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Flow cytometry and Transwell assays, respectively. All protein expression levels were detected by western blot. Tumor xenografts were implemented to explore the role of TUG1 in vivo. Results:We found that there was a marked rise in TUG1 expression in HCC tissues and cells, and knockdown of TUG1 repressed the growth and metastasis and promoted apoptosis of HCC cells. In particular, TUG1 could act as a ceRNA, effectively becoming a sink for miR-216b-5p to fortify the expression of DLX2. Additionally, repression of TUG1 impared the progression of HCC cells by inhibiting DLX2 expression via sponging miR-216b-5p in vitro. More importantly, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-216b-5p via inactivation of the DLX2.Conclusion: TUG1 interacting with miR-216b-5p contributed to proliferation, metastasis, tumorigenesis and retarded apoptosis by activation of DLX2 in HCC.

show abstract

“…Of the oncogenic lncRNAs, VEGF expression is increased by ROR [ 61 ] and TUG1 [ 68 ]. The oncogenic effect of LINC01234 through the effect on the HIF-2α pathway has also been reported [ 108 ].…”

Section: Effect Of Lncrnas On Key Pathways and Processes In Ccrccmentioning

confidence: 99%

LncRNAs in the Regulation of Genes and Signaling Pathways through miRNA-Mediated and Other Mechanisms in Clear Cell Renal Cell Carcinoma

Брага

Фридман

Филиппова

et al. 2021

IJMS

View full text Add to dashboard Cite

The fundamental novelty in the pathogenesis of renal cell carcinoma (RCC) was discovered as a result of the recent identification of the role of long non-coding RNAs (lncRNAs). Here, we discuss several mechanisms for the dysregulation of the expression of protein-coding genes initiated by lncRNAs in the most common and aggressive type of kidney cancer—clear cell RCC (ccRCC). A model of competitive endogenous RNA (ceRNA) is considered, in which lncRNA acts on genes through the lncRNA/miRNA/mRNA axis. For the most studied oncogenic lncRNAs, such as HOTAIR, MALAT1, and TUG1, several regulatory axes were identified in ccRCC, demonstrating a number of sites for various miRNAs. Interestingly, the LINC00973/miR-7109/Siglec-15 axis represents a novel agent that can suppress the immune response in patients with ccRCC, serving as a valuable target in addition to the PD1/PD-L1 pathway. Other mechanisms of action of lncRNAs in ccRCC, involving direct binding with proteins, mRNAs, and genes/DNA, are also considered. Our review briefly highlights methods by which various mechanisms of action of lncRNAs were verified. We pay special attention to protein targets and signaling pathways with which lncRNAs are associated in ccRCC. Thus, these new data on the different mechanisms of lncRNA functioning provide a novel basis for understanding the pathogenesis of ccRCC and the identification of new prognostic markers and targets for therapy.

show abstract

Knockdown of TUG1 by shRNA inhibited renal cell carcinoma formation by miR-299–3p/VEGF axis in vitro and in vivo

Cited by 21 publications

References 24 publications

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

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

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

LncRNAs in the Regulation of Genes and Signaling Pathways through miRNA-Mediated and Other Mechanisms in Clear Cell Renal Cell Carcinoma

Contact Info

Product

Resources

About