LncRNA TUG1 interacting with miR-144 contributes to proliferation, migration and tumorigenesis through activating the JAK2/STAT3 pathway in hepatocellular carcinoma

Lv, Jun; Kong, Yongkui; Gao, Zhiqiang; Liu, Yanmin; Zhu, Pengfei; Yu, Zujiang

doi:10.1016/j.biocel.2018.05.010

Cited by 76 publications

(54 citation statements)

References 39 publications

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“…Interestingly, we found that STAT3 protein acted as the target of miR‐519d, constituting the CASC9‐miR‐519d‐STAT3 axis. STAT3 acts as a transcription factor . With the assistance of bioinformatic JASPAR tool, STAT3 could also bind with the promoter region of lncRNA CASC9, in turn, promoting the transcription activity of lncRNA CASC9.…”

Section: Discussionmentioning

confidence: 99%

“…STAT3 acts as a transcription factor. [26][27][28][29] With the assistance of bioinformatic JASPAR tool, STAT3 could also bind with the promoter region of lncRNA CASC9, in turn, promoting the transcription activity of lncRNA CASC9. Therefore, we conclude that CASC9 relieves the inhibition of STAT3 induced by miR-519d to recover STAT3 expression, reversely, STAT3 could activate the transcription activity of CASC9, forming the positive feedback loop of STAT3-CASC9-miR-519d-STAT3 axis.…”

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Liu

Yang

et al. 2018

J Cellular Molecular Medi

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Emerging evidence have illustrated the vital roles of long noncoding RNAs (lncRNAs) in glioma. Nevertheless, the majority of their roles and mechanisms in gliomagenesis are still largely unclear. In this study, we investigate the roles of lncRNA CASC9 on glioma tumourigenesis and authenticate its potential mechanisms. Results manifested that CASC9 was highly expressed in glioma specimens and cells, moreover, the ectopic overexpression was correlated with glioma patients’ clinic. Functional studies found that siRNA‐mediated CASC9 silencing inhibited the proliferative ability, invasion in vitro, and impaired the tumour growth in vivo. Mechanical studies revealed that miR‐519d both targeted the 3′‐UTR of CASC9 and STAT3 mRNA, which was identified by luciferase reporter assay and RNA immunoprecipitation (RIP). Moreover, chromatin immunoprecipitation (ChIP) and luciferase reporter assay revealed that STAT3, an oncogenic transcription factor, could bind with the promoter of CASC9 and activate its transcriptional level. In conclusion, our results concluded that CASC9 promotes STAT3 expression via sponging miR‐519d, in return, STAT3 activate CASC9 transcription, forming a positive feedback loop of CASC9/miR‐519d/STAT3. The novel finding provides a potential therapeutic target for glioma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Liu

Yang

et al. 2018

J Cellular Molecular Medi

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“…30 At the same time, another lncRNA, AX800134 was reported highly expressed in HBVpositive HCC by Koduru group. 32 Taken together, all these discoveries provide evidences for our hypothesis that lncRNA may play important roles in the progression of HCC and lncRNA CCAT1 be an oncogenic factor in HCC. 31 Additionally, a study indicated that lncRNA taurine upregulated FIGURE 4 CCNE1 is a functional downstream target of miR-30c-2-3p.…”

Section: Discussionmentioning

confidence: 77%

Upregulated LncRNA‐CCAT1 promotes hepatocellular carcinoma progression by functioning as miR‐30c‐2‐3p sponge

Zhang

Cai

Jiang

et al. 2019

Cell Biochemistry & Function

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death over the world. It is well studied that long noncoding RNA colon cancer-associated transcript-1 (CCAT1) played important roles in variety of cancers promoting cell proliferation and metastasis by acting as a competing endogenous RNA (ceRNA) of microRNAs. However, whether CCAT1 could regulate HCC by serving as a ceRNA of microRNA remains to be revealed. In this study, we demonstrated that CCAT1 was highly expressed in HCC tissues and remarkably associated with metastasis. With a bioinformatics prediction and functional assay validation, we found a binding site of miR-30c-2-3p on CCAT1, which was important for CCAT1 to promote cell proliferation. Interestingly, we further revealed a novel recognition site for miR-30c-2-3p on the 3′UTR of CCNE1 by mutative method, luciferase assay, and cell viability confirmation. In general, CCAT1 regulate the expression of CCNE1 by acting as a ceRNA to sponge miR-30c-2-3p in regulating the cell proliferation of HCC. These results suggest that CCAT1 may be a new therapy target for HCC in the future.Significance of the study: Our findings may broaden the understanding of the role of CCAT1 in tumorigenesis and may provide a new therapy target for HCC.

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“…Wang et al, 2017). In human hepatocellular carcinoma, TUG1 promotes cell migration and invasion via interacting with miR-144 and activating the JAK2/STAT3 pathway (Lv et al, 2018). Functionally, we validated the promotion of TUG1 in human adenomyosis.…”

Section: Timp2 Is Potentially Involved In Adenomyotic Epithelial Cementioning

confidence: 71%

“…In human osteosarcoma, TUG1 functions as a competitive endogenous RNA with miR‐335‐5p and regulates ROCK1‐mediated migration and invasion (Y. Wang et al, ). In human hepatocellular carcinoma, TUG1 promotes cell migration and invasion via interacting with miR‐144 and activating the JAK2/STAT3 pathway (Lv et al, ). Functionally, we validated the promotion of TUG1 in human adenomyosis.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of long noncoding RNA TUG1 by EGR1 promotes adenomyotic epithelial cell migration and invasion through recruiting EZH2 and suppressing TIMP2

Shi

Sha

et al. 2019

Molecular Reproduction Devel

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Emerging studies showed that lncRNA taurine upregulated 1 (TUG1) plays important roles in diverse biological processes. However, there is no previously published research reporting the regulatory role of lncRNAs in the progression of adenomyosis. In the present study, we found that TUG1 is upregulated in human adenomyosis, and the overexpression of TUG1 is associated with the transcription factor early growth response 1 (EGR1). Functionally, the knockdown of TUG1 inhibited adenomyotic epithelial cell migration and invasion but not growth. The mechanistic experiments demonstrated that the function of TUG1 in adenomyotic epithelial cell invasion is, at least in part, through recruiting the enhancer of zeste homolog 2 (EZH2) to the promoter of tissue inhibitor of metalloproteinases 2 (TIMP2) and negatively regulating its expression. Our study demonstrated that TUG1 promotes the migration and invasion of human adenomyotic epithelial cells, and EGR1/TUG1/EZH2/TIMP2 may be a potential therapeutic target for adenomyosis.

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LncRNA TUG1 interacting with miR-144 contributes to proliferation, migration and tumorigenesis through activating the JAK2/STAT3 pathway in hepatocellular carcinoma

Cited by 76 publications

References 39 publications

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Long noncoding RNA CASC9/miR‐519d/STAT3 positive feedback loop facilitate the glioma tumourigenesis

Upregulated LncRNA‐CCAT1 promotes hepatocellular carcinoma progression by functioning as miR‐30c‐2‐3p sponge

Upregulation of long noncoding RNA TUG1 by EGR1 promotes adenomyotic epithelial cell migration and invasion through recruiting EZH2 and suppressing TIMP2

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