Long noncoding RNA 91H overexpression contributes to the growth and metastasis of HCC by epigenetically positively regulating IGF2 expression

Yi, Tingzhuang; Wang, Tonghua; Shi, Ying; Peng, Xiaojuan; Tang, Shaohui; Zhong, Lina; Chen, Yanfang; Li, Yuting; He, Kaiyin; Wang, Min; Zhao, Hailiang; Li, Qing

doi:10.1111/liv.14300

Cited by 18 publications

(11 citation statements)

References 38 publications

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“…It is predominantly expressed from the maternal allele in human and mouse within the H19 gene region. In HCC tissue and cells, 91H is overexpressed [42]. High 91H expression is associated with a poor prognosis in HCC patients: both disease-free survival time and the overall survival time was shorter compared to patients with low 91H expressions [42].…”

Section: Lncrna 91hmentioning

confidence: 95%

“…In HCC tissue and cells, 91H is overexpressed [42]. High 91H expression is associated with a poor prognosis in HCC patients: both disease-free survival time and the overall survival time was shorter compared to patients with low 91H expressions [42]. In vitro studies revealed that a knockdown of 91H in Hep3B cells down-regulated the expression of insulin-like growth factor 2 (IGF2) suggesting a co-regulation of 91H and IGF2 [42].…”

Section: Lncrna 91hmentioning

confidence: 99%

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The Good, the Bad, the Question–H19 in Hepatocellular Carcinoma

Tietze

Kessler

2020

Cancers

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Hepatocellular carcinoma (HCC), the most common primary liver cancer, is challenging to treat due to its typical late diagnosis, mostly at an advanced stage. Therefore, there is a particular need for research in diagnostic and prognostic biomarkers and therapeutic targets for HCC. The use of long noncoding (lnc) RNAs can widen the list of novel molecular targets improving cancer therapy. In hepatocarcinogenesis, the role of the lncRNA H19, which has been known for more than 30 years now, is still controversially discussed. H19 was described to work either as a tumor suppressor in vitro and in vivo, or to have oncogenic features. This review attempts to survey the conflicting study results and tries to elucidate the potential reasons for the contrary findings, i.e., different methods, models, or readout parameters. This review encompasses in vitro and in vivo models as well as studies on human patient samples. Although the function of H19 in HCC remains elusive, a short outlook summarizes some ideas of using the H19 locus as a novel target for liver cancer therapy.

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Section: Lncrna 91hmentioning

confidence: 95%

Section: Lncrna 91hmentioning

confidence: 99%

The Good, the Bad, the Question–H19 in Hepatocellular Carcinoma

Tietze

Kessler

2020

Cancers

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“…Consequently, LINRIS knockdown weakens downstream effects of IGF2BP2, particularly MYC-mediated glycolysis in CRC cells and proliferation of cancer cells. On the other hand, lncRNA 91H, a long non-coding antisense transcript located at H19/IGF2 locus, participates in tumor development [101,102]. lncRNA 91H silencing modulates proliferation, migration, invasion, autophagy and expression of mammalian target of rapamycin (mTOR) in CRC cancer cells by suppressing IGF2 expression, which up-regulates the expression of IGF2BP2 [103].…”

Section: Igf2bp2 and Lncrnas In Cancersmentioning

confidence: 99%

The role of IGF2BP2, an m6A reader gene, in human metabolic diseases and cancers

2021

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The human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2/IMP2) is an RNA-binding protein that regulates multiple biological processes. Previously, IGF2BP2 was thought to be a type 2 diabetes (T2D)-associated gene. Indeed IGF2BP2 modulates cellular metabolism in human metabolic diseases such as diabetes, obesity and fatty liver through post-transcriptional regulation of numerous genes in multiple cell types. Emerging evidence shows that IGF2BP2 is an N6-methyladenosine (m6A) reader that participates in the development and progression of cancers by communicating with different RNAs such as microRNAs (miRNAs), messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs). Additionally, IGF2BP2 is an independent prognostic factor for multiple cancer types. In this review, we summarize the current knowledge on IGF2BP2 with regard to diverse human metabolic diseases and its potential for cancer prognosis.

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“…In recent years, a number of studies have reported that aberrant expression of lncRNAs is related to hepatocarcinogenesis [15][16][17]. LncRNAs, a heterogeneous group of RNA transcripts with a length of more than 200 nucleotides, are generally regarded as lacking proteincoding roles [3].…”

Section: Discussionmentioning

confidence: 99%

Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2

Zhou

Luo

et al. 2021

J Exp Clin Cancer Res

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Background Increasing evidence has demonstrated that long noncoding RNAs (lncRNAs) have regulatory functions in hepatocellular carcinoma (HCC). The link between lincSCRG1 and HCC remains unclear. Methods To explore the lincSCRG1 regulation axis, bioinformatics, RIP and luciferase reporter assay were performed. The expressions of lincSCRG1-miR26a-SKP2 were detected in HCC tissues and cell lines through qPCR and western blot. The functions of HCC cells were investigated through in vitro assays (MTT, colony formation, transwell and flow cytometry) and the inner effect of lincSCRG1-miR26a in vivo was evaluated by xenografts and liver metatstatic nude mice models. Results LincSCRG1 was found to be strongly elevated in human HCC tissues and cell lines. MiR26a and S phase kinase-related protein 2 (SKP2) were predicted as the target miRNA for lincSCRG1 and the target gene for miR26a with direct binding sites, respectively. LincSCRG1 was verified as a competing endogenous RNA (ceRNA) via negative regulation of miR26a and derepression of SKP2 in HCC cells. Both overexpression of lincSCRG1 (ov-lincSCRG1) and inhibition of miR26a (in-miR26a) obviously stimulated cellular viability, colony formation, migration and proliferation of S phase cells and also significantly increased the protein levels of cyclinD1, CDK4, MMP2/3/9, Vimentin, and N-cadherin or inhibited the protein level of E-cadherin of HCC cells, while knockdown of lincSCRG1 (sh-lincSCRG1) and upregulation of miR26a (mi-miR26a) had the opposite effects on HCC cells. Cotransfection of in-miR26a or overexpression of SKP2 (ov-SKP2) with sh-lincSCRG1 could rescue the anticancer functions of sh-lincSCRG1, including suppressing proliferation and migration of HCC cells. Additionally, sh-lincSCRG1 could effectively inhibit the growth of subcutaneous xenograft tumours and lung metastasis, while the anticancer effect of sh-lincSCRG1 could be reversed by cotransfection of in-miR26a. Conclusions LincSCRG1 acts as a ceRNA of miR26a to restrict its ability to derepress SKP2, thereby inducing the proliferation and migration of HCC cells in vitro and in vivo. Depletion of lincSCRG1 could be used as a potential therapeutic approach in HCC.

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Long noncoding RNA 91H overexpression contributes to the growth and metastasis of HCC by epigenetically positively regulating IGF2 expression

Cited by 18 publications

References 38 publications

The Good, the Bad, the Question–H19 in Hepatocellular Carcinoma

The Good, the Bad, the Question–H19 in Hepatocellular Carcinoma

The role of IGF2BP2, an m6A reader gene, in human metabolic diseases and cancers

Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2

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