Long noncoding RNA TUG1 promotes cell proliferation and migration of renal cell carcinoma via regulation of YAP

Liu, Shan; Yang, Yuxin; Wang, Weiwei; Pan, Xiaoyue

doi:10.1002/jcb.27284

Cited by 47 publications

(32 citation statements)

References 39 publications

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“…23 Previous studies have reported that LINC00339 is the sponge for miR-377-3p, miR-145, and miR-539-5p. [12][13][14] This work for the first time identified LINC00339 as the sponge for miR-1182. To date, knowledge about miR-1182 is poor.…”

Section: Discussionmentioning

confidence: 81%

“…21 Recently, several researchers have demonstrated that LINC00339 promotes proliferation, migration, and invasion of laryngeal squamous cell carcinoma and breast cancer. 13,14 Its role in HCC remains limitedly studied. We provided evidence that LINC00339 promotes HCC tumorigenesis and metastasis through the miR-1182/ SKA1 pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Previously, researchers have shown that LINC00339 promotes the development of glioma and laryngeal squamous cell carcinoma. [12][13][14] However, the roles of LINC00339 in HCC are unclear. Our research indicated that LINC00339 was upregulated in HCC tissues.…”

Section: Introductionmentioning

confidence: 99%

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<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

Xiao¹,

Yu²,

Ma³

2019

OTT

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Background: Extensive research has shown that long noncoding RNA (lncRNA) is involved in tumorigenesis, including hepatocellular carcinoma (HCC). The lncRNA LINC00339 was reported to regulate the development of lung cancer or breast cancer. However, whether LINC00339 participates in HCC progression remains unclear. Here, our results showed that LINC00339 was upregulated in HCC. Methods: qRT-PCR and in situ hybridization (ISH) was used to analyze LINC00339 expression in tumor tissues and cell lines. CCK8 and colony formation assays were used to analyze cell proliferation. Transwell assay was used to analyze cell migration and invasion. Xenograft experiment was used to test tumor growth in vivo. Results: LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis in HCC patients. Functional investigation showed that LINC00339 knockdown significantly suppressed HCC cell proliferation, migration, and invasion. Moreover, decreased LINC00339 expression inhibited HCC growth in vivo. Mechanistically, LINC00339 could interact with miR-1182 to promote SKA1 expression. We also demonstrated that SKA1 acted as an oncogene and SKA1 upregulation reversed the effect of LINC00339 silencing. Conclusion: Our results illustrated that the LINC00339/miR-1182/SKA1 axis plays an essential role in HCC progression.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

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<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

Xiao¹,

Yu²,

Ma³

2019

OTT

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“…30 A study has showed that downregulated lncRNA taurine-up-regulated gene 1 (TUG1) occurs with decreased YAP levels. 31 A new study has noted that Beclin1 works in autophagy via complexes like the Beclin1-PI3KC3 or Beclin1-Bcl-2 complex. 32 LC3II was considered as an autophagy-linked marker in cell tissues.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

Peng

Tan

et al. 2019

J Cellular Molecular Medi

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The role of long non‐coding RNAs (lncRNAs) in thyroid carcinoma (TC), the most frequent endocrine malignancy, has been extensively examined. This study investigated effect of interaction among lncRNA TNRC6C‐AS1, serine/threonine‐protein kinase 4 (STK4) and Hippo signalling pathway on TC. Initially, lncRNA TNRC6C‐AS1 expression in TC tissues was detected. To explore roles of lncRNA TNRC6C‐AS1, STK4 and Hippo signalling pathway in TC progression, their expressions were altered. Interaction between lncRNA TNRC6C‐AS1 and STK4, STK4 promoter methylation, or Hippo signalling pathway was verified. After that, a series of experiments were employed to evaluate in vitro ability of apoptosis, proliferation and autophagy of TC cells and in vivo tumorigenicity, and tumour growth of TC cells. lncRNA TNRC6C‐AS1 was highly expressed while STK4 was poorly expressed in TC tissues. LncRNA TNRC6C‐AS1 promoted the STK4 methylation and down‐regulated STK4 expression, which further activated the Hippo signalling pathway. STK4 silencing was observed to promote the proliferation ability of TC cells, inhibit the apoptosis and autophagy abilities, as well as enhance the tumorigenicity and tumour growth. Moreover, the in vitro proliferation ability as well as the in vivo tumorigenicity and tumour growth of TC cells were inhibited after the blockade of Hippo signalling pathway, while the apoptosis and autophagy abilities were promoted. The results demonstrate that the lncRNA TNRC6C‐AS1 increases STK4 promoter methylation to down‐regulate STK4 expression, thereby promoting the development of TC through activation of Hippo signalling pathway. It highlights that lncRNA TNRC6C‐AS1 may be a novel therapeutic target for the treatment of TC.

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“…LncRNA THOR mediated the progression of retinoblastoma through regulating c-myc and IGF2BP1 [18] . In addition, TUG1 has been reported to target YAP to regulate cell proliferation and migration of renal cell carcinoma [19] . In the present study, our result revealed that TUG1 mediated periprosthetic osteolysis by directly targeting BMP-7.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Long Non-coding RNA TUG1 Suppresses Osteoblast Apoptosis in Particle-induced Osteolysis by Up-regulating BMP-7

Wu¹,

Liu²

2018

Clin Surg Res Commun

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Background: Periprosthetic osteolysis may lead to the failure of hip arthroplasty. The role of long non-coding RNA TUG1 in inducing periprosthetic osteolysis after hip arthroplasty remains unknown. Methods: Clinical tissues were obtained from the patients undergoing hip arthroplasty. Mouse osteoblast cell line MC3T3-E1 was simulated by CoCrMo metal particles (CoPs). Real-time PCR was performed to determine the expression of TUG1 and BMP-7. Western blot was performed to determine the BMP-7 protein expression. Cell apoptosis was determined using flow cytometry. RNA pull-down was performed to determine the interaction between TUG1 and BMP-7. In vivo experiments were performed to verify the role of TUG1. Results: Overexpressed TUG1 and down-regulated BMP-7 was observed in both clinical periprosthetic tissues and CoPs-stimulated osteoblasts. Knockdown of TUG1 significantly inhibited the apoptosis of CoPs-stimulated osteoblasts by targeting BMP-7. In vivo experiments verified that knockdown of TUG1 increased bone mineral density of the mouse osteolysis model. Conclusion: Knockdown of TUG1 inhibited the apoptosis of CoPs-stimulated osteoblasts by negatively regulating BMP-7, which might provide a new insight in treating periprosthetic osteolysis after hip arthroplasty.

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Long noncoding RNA TUG1 promotes cell proliferation and migration of renal cell carcinoma via regulation of YAP

Abstract: Our findings indicated a pivotal role of TUG1 in driving RCC progression via regulation of miR-9/YAP, suggesting a potential therapeutic targeting role of TUG1 in RCC.

Cited by 47 publications

References 39 publications

<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

<p>LINC00339 promotes growth and invasiveness of hepatocellular carcinoma by the miR-1182/SKA1 pathway</p>

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

Knockdown of Long Non-coding RNA TUG1 Suppresses Osteoblast Apoptosis in Particle-induced Osteolysis by Up-regulating BMP-7

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