An LTR Retrotransposon-Derived Long Noncoding RNA lncMER52A Promotes Hepatocellular Carcinoma Progression by Binding p120-Catenin

Wu, Yangjun; Zhao, Yiming; Huan, Lin; Zhao, Jingjing; Zhou, Yuqiang; Xu, Linguo; Hu, Zhixiang; Liu, Yizhe; Chen, Zhiao; Wang, Lu; Huang, Shenglin; He, Xianghuo; Liang, Linhui

doi:10.1158/0008-5472.can-19-2115

Cited by 51 publications

(44 citation statements)

References 45 publications

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“…The malignant transformation of tumor is mainly related to over-activation or over-expression of Rac1. Up to now, the increase of Rac1 expression has been detected in different types of cancers, such as BC, lung cancer, colorectal cancer, gastric cancer, prostate cancer, hepatocellular carcinoma and ovarian cancer (40)(41)(42)(43)(44)(45)(46). The activity of Rac1 is also related to many posttranslational modifications, such as phosphorylation (Tyr64, Ser71), ubiquitination (Lys147, K166R), lipidation, and adenylation (Y32) (47)(48)(49)(50)(51)(52)(53).…”

Section: The Expression and Clinical Significance Of Rac1 In Tumorsmentioning

confidence: 99%

Rac1, A Potential Target for Tumor Therapy

et al. 2021

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RAS-related C3 botulinum toxin substrate 1 (Rac.1) is one of the important members of Rho GTPases. It is well known that Rac1 is a cytoskeleton regulation protein that regulates cell adhesion, morphology, and movement. Rac1 is highly expressed in different types of tumors, which is related to poor prognosis. Studies have shown that Rac1 not only participates in the tumor cell cycle, apoptosis, proliferation, invasion, migration and angiogenesis, but also participates in the regulation of tumor stem cell, thus promoting the occurrence of tumors. Rac1 also plays a key role in anti-tumor therapy and participates in immune escape mediated by the tumor microenvironment. In addition, the good prospects of Rac1 inhibitors in cancer prevention and treatment are exciting. Therefore, Rac1 is considered as a potential target for the prevention and treatment of cancer. The necessity and importance of Rac1 are obvious, but it still needs further study.

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Section: The Expression and Clinical Significance Of Rac1 In Tumorsmentioning

confidence: 99%

Rac1, A Potential Target for Tumor Therapy

et al. 2021

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“…The results reported here that YY1 has importance in promoting hepatocarcinogenesis is consistent with the previous reports. Wu et al showed YY1 transcription factor promoted HCC progression by activating lncMER52A and then stabilized p120-catenin the downstream effector of lncMER52A [25] . YY1 promoted HCC cells proliferation and migration via facilitating linc01134/miR-324-5p/IGF2BP1, and IGF2BP1 stabilizing YY1 mRNA expression, forming a positive feedback loop [26] .…”

Section: Discussionmentioning

confidence: 99%

“…After treated with or without VE821 for 48 h, MHCC-97H cells in different dish were added with cycloheximide (CHX, 50 g/ml) at the same time. At indicted time points (0, 5,10,15,20,25,30,35,40 and 45 h), protein samples were collected and then analyzed by western blotting assay.…”

Section: Protein Degradation Analysismentioning

confidence: 99%

The Rna-binding Protein GRSF1 Promote shepatocarcinogenesis via competitively Binding Toyy1 mRNA with mIR-30e-5p

Han

Wang

et al. 2020

Preprint

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Background:Numerous studies have highlighted that dysregulation of RNA binding protein (RBP) expression is causally linked with human cancer tumorigenesis. The detailed biological effect and underlying mechanisms of RBP GRSF1 in hepatocellular carcinoma (HCC) remain unclear.Methods:GRSF1 expression in HCC tissues and cells was measured by western blotting and qRT-PCR assays. HCC cells with stable knockdown of GRSF1 were established using two sh-RNA encoding lentiviruses. Then the functions of GRSF1 in HCC were explored using MTT, colony formation, flow cytometry, Transwell assays and xenograft model. Transcriptometric sequencing in GRSF1-deficient MHCC-97H cells were carried out to identify the downstream effector of GSRF1. The regulatory mechanisms among GRSF1, YY1 and miR-30e-5p were investigated by RNA immunoprecipitation, luciferase assay, RNA pull down and ChIP assay.Results:GRSF1was frequently increased in HCC tissue and cells with a worse clinical outcomes in HCC. GRSF1 worked as a novel oncogenic RBP in vitro and in vivo via post-regulating the stability of YY1 mRNA. And the GUUU motifs on YY1 3`UTR 2663-2847 was the specific binding motifs for GRSF1. More interesting, YY1 feedback promoted GRSF1 expression by binding to GRSF1 promoters. In addition, YY1 was a critical target of miR-30e-5p, which was confirmed by our data that inhibited HCC hepatocarcinogenesis. Further investigation showed GRSF1 and miR-30e-5p competitively regulated YY1 via binding to its YY1 3`UTR 2663-2847 region. At last, we identified that 3-amino-6-(4-methylsulfonylphenyl)-N-phenylpyrazine-2-carboxamide (VE821) blocked HCC progression by inhibiting the GRSF1/YY1 pathway.Conclusions:GRSF1 promoted hepatocarcinogenesis via competitively binding to YY1 3`UTR 2663-2847 with miR-30e-5p.The interaction network among GRSF1, YY1 and miR-30e-5p provided a new insight for the HCC pathogenesis, and VE821 may serve as a novel agent with potential for HCC treatment via inhibiting GRSF1/YY1 axis.

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“…A third significant aspect of HERV reactivation is associated with the expression of long noncoding RNAs (lncRNAs), as recently observed in hepatocellular carcinoma ( Table 2 ) [ 27 , 34 ].…”

Section: Human Endogenous Retrovirusesmentioning

confidence: 99%

“…Indeed, HCC development is a multistep process associated with genetic alterations, as well as dysregulated gene expression. However, recent findings indicate a dysregulated expression of LTR-derived noncoding RNAs (ncRNAs) in HCC [ 27 , 34 ].…”

Section: Hervs and Liver Cancermentioning

confidence: 99%

Human Endogenous Retrovirus Reactivation: Implications for Cancer Immunotherapy

Petrizzo

Ragone

Cavalluzzo

et al. 2021

Cancers

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Human endogenous retroviruses (HERVs) derive from ancestral exogenous retroviruses whose genetic material has been integrated in our germline DNA. Several lines of evidence indicate that cancer immunotherapy may benefit from HERV reactivation, which can be induced either by drugs or by cellular changes occurring in tumor cells. Indeed, several studies indicate that HERV proviral DNA can be transcribed either to double-stranded RNA (dsRNA) that is sensed as a “danger signal” by pattern recognition receptors (PRRs), leading to a viral mimicry state, or to mRNA that is translated into proteins that may contribute to the landscape of tumor-specific antigens (TSAs). Alternatively, HERV reactivation is associated with the expression of long noncoding RNAs (lncRNAs). In this review, we will highlight recent findings on HERV reactivation in cancer and its implications for cancer immunotherapy.

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An LTR Retrotransposon-Derived Long Noncoding RNA lncMER52A Promotes Hepatocellular Carcinoma Progression by Binding p120-Catenin

Cited by 51 publications

References 45 publications

Rac1, A Potential Target for Tumor Therapy

Rac1, A Potential Target for Tumor Therapy

The Rna-binding Protein GRSF1 Promote shepatocarcinogenesis via competitively Binding Toyy1 mRNA with mIR-30e-5p

Human Endogenous Retrovirus Reactivation: Implications for Cancer Immunotherapy

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