Retracted: micro<scp>RNA</scp>‐497 inhibits cell proliferation and induces apoptosis by targeting <scp>YAP</scp>1 in human hepatocellular carcinoma

Zhang, Lei; Yu, Zhaoxiang; Xian, Yuezhong; Lin, Xiaolan

doi:10.1002/2211-5463.12032

Cited by 28 publications

(29 citation statements)

References 26 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown that miR-497 can act as a tumor suppressor, including in HCC. 24,25 The regulatory relationship between LINC02476 and miR-497 was confirmed by the following data: 1) LINC02476 downregulation increased the expression of miR-497; 2) a luciferase activity assay confirmed the direct binding to the predicted miR-497 binding site on LINC02476; 3) the RIP assay confirmed thatLINC02476 and miR-497 were in the same RNAinduced silencing complex. In our study, HMGA2 was identified as a downstream target of miR-497.…”

mentioning

confidence: 73%

LINC02476 Promotes the Malignant Phenotype of Hepatocellular Carcinoma by Sponging miR-497 and Increasing HMGA2 Expression

Duan¹,

Zhao²,

Jiang³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Long noncoding RNAs (lncRNAs) can promote hepatocellular carcinoma (HCC) initiation and progression. In this report, we examined the role of lncRNA LINC02476 in HCC. Methods: The expression levels of different lncRNAs in HCC were explored using the TCGA database and lncRNA LINC02476 was selected for further study. The expression of LINC02476 in HCC tissues was determined by real-time PCR. The clinicopathological characteristics of HCC patients were analyzed relative to the expression of LINC02476. The expression of LINC02476 was downregulated in HCC cells using a lentiviral vector and different assays were performed to study cell growth, proliferation, invasion, apoptosis and the cell cycle. MiR-497 was selected as a miRNA that could interact with LINC02476 which was further tested by RNA immunoprecipitation. HMGA2 was selected as a possible target of miR-497, and their interaction was examined by a luciferase reporter assay. Results: LINC02476 expression was elevated in HCC cell lines and HCC tissues. When LINC02476 was downregulated, the growth and the invasion of HCC cells decreased in vitro and in vivo. LINC02476 negatively regulated the expression of miR-497 by acting as a ceRNA. HMGA2 was directly targeted and inhibited by miR-497. Conclusion: The results indicate that LINC02476 functions through the miR-497/HMGA2 axis and that it has a role in the growth and metastasis of HCC cells. Therefore, LINC02476 could be an interesting new molecular target in HCC therapies.

show abstract

mentioning

confidence: 73%

LINC02476 Promotes the Malignant Phenotype of Hepatocellular Carcinoma by Sponging miR-497 and Increasing HMGA2 Expression

Duan¹,

Zhao²,

Jiang³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…YAP1 was upregulated in HCC tissues and cells, and promoted HCC development and progression [24]. In addition, recently miR-497 and miR-506 were reported to inhibit cell proliferation and induce apoptosis by targeting YAP1 in HCC [31, 32]. Therefore, we speculated that miR-199a-3p might target YAP1 to regulate HCC cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

miR-199a-3p inhibits cell proliferation and induces apoptosis by targeting YAP1, suppressing Jagged1-Notch signaling in human hepatocellular carcinoma

Ren

Zhang

et al. 2016

J Biomed Sci

View full text Add to dashboard Cite

BackgroundmiR-199a-3p was significantly downregulated in the majority of human hepatocellular carcinoma (HCC) tissues and HCC cell lines. Yes associated protein 1 (YAP1) was overexpressed in human HCC, which promoted HCC development and progression by upregulating Jagged1 and activating the Notch pathway. We searched potential targets of miR-199a-3p with DIANA, TargetScan and PicTar tools, and found that YAP1 is one of the potential targets. Based on these findings, we speculated that miR-199a-3p might suppress HCC growth by targeting YAP1, downregulating Jagged1 and suppressing the Notch pathway.ResultsWe determined the expression of miR-199a-3p and YAP1 by quantitative Real-Time PCR (qRT-PCR) and western blot assays, respectively, and found downregulation of miR-199a-3p and upregulation of YAP1 in HCC cell lines. Cell proliferation and apoptosis assays showed that miR-199a-3p suppresses HCC cell proliferation and promotes apoptosis, and knockdown of YAP1 has similar role. Furthermore, we verified that miR-199a-3p can directly target YAP1. We further investigated and confirmed that miR-199a-3p and YAP1 regulate HCC cell proliferation and apoptosis through Jagged1-Notch signaling.ConclusionmiR-199a-3p targets YAP1, downregulates Jagged1 and suppresses the Notch signaling to inhibit HCC cell proliferation and promote apoptosis. These findings provide new insights into the mechanism by which miR-199a-3p suppresses HCC cell proliferation and induces apoptosis.

show abstract

“…Analyses of TargetScan database and previous studies [16,17,32,33] revealed that 3' UTRs of YAP, SMAD3, CCND1 and BIRC5 contained at least one conserved binding site for miR-497 ~ 195 cluster (Fig. 4B).…”

Section: Mir-497 and Mir-195 Directly Suppressed Multiple Key Componementioning

confidence: 59%

LncRNA MIR497HG suppresses bladder cancer progression through disrupting the crosstalk between Hippo/Yap and TGF-β/Smad signaling

Zhuang

Liu

Yuan

et al. 2020

Preprint

View full text Add to dashboard Cite

Objectives A subclass of long non-coding RNAs (lncRNAs), categorized as miRNA-host gene lncRNAs (lnc-miRHGs), is processed to produce miRNAs and involve in cancer progression. This work aimed to investigate the influence and the molecular mechanisms of lnc-miRHGs MIR497HG in bladder cancer (BCa). Materials and methods The miR-497 and miR-195 were derived from MIR497HG. Cell proliferation, migration and invasion assays were used to measure the function of MIR497HG, miR-497 and miR-195 in BCa. Bioinformatics, RT-qPCR, western blot, luciferase reporter assay, ChIP, and so on, were used to reveal the upstream and downstream mechanisms of MIR497HG in BCa. Results We identified that lnc-miRHG MIR497HG and two harbored miRNAs, miR-497 and miR-195, were downregulated in BCa by analyzing TCGA and our dataset. MIR497HG overexpression inhibited BCa cell proliferation, migration and invasion in vitro. MiR-497/miR-195 inhibitor rescued significantly the inhibiton effects of overexpression of MIR497HG in BCa. Mechanistically, miR-497 and miR-195 coordinately suppressed multiple key components in Hippo/Yap and TGF-β signaling, and particularly attenuated the interaction between Yap and Smad3. In addition, E2F4 was proved to be critical for silencing MIR497HG transcription in BCa cells. Conclusions We propose for the first time that MIR497HG suppressed BCa progression and its upstream and downstream mechanisms. Blocking the pathological process may be a potential strategy for the treatment of BCa.

show abstract

Retracted: microRNA‐497 inhibits cell proliferation and induces apoptosis by targeting YAP1 in human hepatocellular carcinoma

Cited by 28 publications

References 26 publications

<p>LINC02476 Promotes the Malignant Phenotype of Hepatocellular Carcinoma by Sponging miR-497 and Increasing HMGA2 Expression</p>

<p>LINC02476 Promotes the Malignant Phenotype of Hepatocellular Carcinoma by Sponging miR-497 and Increasing HMGA2 Expression</p>

miR-199a-3p inhibits cell proliferation and induces apoptosis by targeting YAP1, suppressing Jagged1-Notch signaling in human hepatocellular carcinoma

LncRNA MIR497HG suppresses bladder cancer progression through disrupting the crosstalk between Hippo/Yap and TGF-β/Smad signaling

Contact Info

Product

Resources

About