LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

Jiang, Wenjin; Cheng, Xueling; Wang, Tao; Xue-peng, Song; Zheng, Yanbo; Wang, Ligang

doi:10.1002/jgm.3134

Cited by 34 publications

(33 citation statements)

References 27 publications

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“…SNHG11 promotes proliferation and metastasis by targeting the Hippo pathway in colorectal cancer and may act as diagnostic markers for the detection of pancreatic cancer and prostate cancer. [11][12][13] Recent studies have shown that lncRNA regulates cell proliferation, apoptosis, metastasis, invasion, angiogenesis, lipid metabolism, EMT, and many other processes, and has an impact on tumor size, TNM grade, postoperative survival, and prognosis of HCC. 8,[14][15][16] Bioinformatics analysis and luciferase reporter assay found that the binding site of SNHG11 is miR-184 and miR-184 directly targets AGO2.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG11 Promotes Proliferation, Migration, Apoptosis, and Autophagy by Regulating hsa-miR-184/AGO2 in HCC</p>

Huang

Zhao

et al. 2020

OTT

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Background: The most common malignant tumor of the digestive system is HCC. However, the mechanism and pathogenesis of HCC occurrence and progress are still unknown. LncRNA is closely related to the occurrence and progress of HCC. It is important to investigate the effect and role of lncRNA in HCC. Materials and Methods: LncRNA microarray assay was used to screen the differential expression profile of lncRNA. SNHG11, miR-184 and GO2 expression was analyzed by RT-PCR. The ability of SNHG11 to serve as a sponge for miRNA and the fact that miR-184 directly targets mRNA were revealed by dual luciferase assay and RIP. Apoptosis and autophagy related proteins were detected by Western blot. Cell proliferation, invasion, migration, and apoptosis were detected by CCK-8 assay, wound healing assay, transwell assay, and flow cytometry. Results: LncRNA microarray assay and RT-PCR results revealed that the expression of SNHG11 was increased in HCC tumor tissues and also upregulated in HCC cells. SNHG11 had a connection with poor survival rate in HCC. In addition, dual luciferase assay and RIP results revealed that SNHG11 serves as a sponge for miR-184 and miR-184 directly targets AGO2. Pearson correlation analysis showed that SNHG11 with miR-184 and miR-184 with AGO2 were negative correlations, and SNHG11 with AGO2 was a positive correlation. Cell function assay and Western blot showed SNHG4/miR-184/AGO2 regulatory loop was critical for HCC cell proliferation, migration, apoptosis, and autophagy. Conclusion: Our study demonstrated that the expression of SNHG11 is higher in HCC; moreover, SNHG11 promotes proliferation, migration, apoptosis, and autophagy by regulating AGO2 via miR-184 in HCC. Our verification of the role of SNHG11 may provide a novel biomarker for the diagnosis, therapy, and prognosis of HCC.

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Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG11 Promotes Proliferation, Migration, Apoptosis, and Autophagy by Regulating hsa-miR-184/AGO2 in HCC</p>

Huang

Zhao

et al. 2020

OTT

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“…LINC00467 binds to the IGF2BP3 protein to stabilize TRAF5 mRNA. LINC00467/IGF2BP3 promotes metastasis hepatocellular carcinoma by retaining TRAF5 mRNA stability [ 104 ]. LINC01225 binds to the EGFR protein and elevates its protein level.…”

Section: Lncrna–protein Interaction In Cancer Developmentmentioning

confidence: 99%

Epigenetic Mechanisms of LncRNAs Binding to Protein in Carcinogenesis

Shin

Lee

Cho

2020

Cancers

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Epigenetic dysregulation is an important feature for cancer initiation and progression. Long non-coding RNAs (lncRNAs) are transcripts that stably present as RNA forms with no translated protein and have lengths larger than 200 nucleotides. LncRNA can epigenetically regulate either oncogenes or tumor suppressor genes. Nowadays, the combined research of lncRNA plus protein analysis is gaining more attention. LncRNA controls gene expression directly by binding to transcription factors of target genes and indirectly by complexing with other proteins to bind to target proteins and cause protein degradation, reduced protein stability, or interference with the binding of other proteins. Various studies have indicated that lncRNA contributes to cancer development by modulating genes epigenetically and studies have been done to determine which proteins are combined with lncRNA and contribute to cancer development. In this review, we look in depth at the epigenetic regulatory function of lncRNAs that are capable of complexing with other proteins in cancer development.

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“…Studies of multiple cancer types have demonstrated that a set of cancer-related pathways, particularly those involved in invasion, may be mediated by IGF2BP3 (13,16). The results of a mechanical study also demonstrated that IGF2BP3 facilitated partial invasion-promoted gene expression and decreased the expression of certain tumor-suppressing genes (20,21). For example, IGF2BP3 has been shown to function as a cytoplasmic 'safehouse' and to prevent the mRNA-directed decay of oncogene Hmga2 during tumorigenesis (22).…”

Section: Introductionmentioning

confidence: 99%

IGF2BP3 and miR191‑5p synergistically increase HCC cell invasiveness by altering ZO‑1 expression

et al. 2020

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Early studies have indicated that insulin-like growth factor II mRNA binding protein 3 (IGF2BP3/IMP3) may affect the progression of hepatocellular carcinoma (HCC); however, the detailed underlying mechanisms, particularly its linkage to tight junction protein-mediated cell invasion, remain unclear. The present study revealed that IGF2BP3 increased HCC cell invasiveness by suppressing zonula occludens-1 (ZO-1) expression, via direct binding to the 3' untranslated region (3'-UTR). Analysis of the molecular mechanisms demonstrated that IGF2BP3 binds to the overlapping targets of IGF2BP3-RNA cross-linkage and microRNA (miR)191-5p targeting sites, and promotes the formation of an miR191-5pinduced RNA-induced silencing complex. The knockdown of IGF2BP3 or the addition of a miR-191-5p inhibitor decreased cellular invasiveness and increased ZO-1 expression. Analysis of the human HCC database also confirmed the association between IGF2BP3 and HCC progression. Collectively, these preclinical findings suggest that IGF2BP3 increases HCC cell invasiveness by promoting the miR191-5p-induced suppression of ZO-1 signaling. This newly identified signaling effect on small molecule targeting may aid in the development of novel strategies with which to inhibit HCC progression more effectively.

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LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

Cited by 34 publications

References 27 publications

<p>LncRNA SNHG11 Promotes Proliferation, Migration, Apoptosis, and Autophagy by Regulating hsa-miR-184/AGO2 in HCC</p>

<p>LncRNA SNHG11 Promotes Proliferation, Migration, Apoptosis, and Autophagy by Regulating hsa-miR-184/AGO2 in HCC</p>

Epigenetic Mechanisms of LncRNAs Binding to Protein in Carcinogenesis

IGF2BP3 and miR191‑5p synergistically increase HCC cell invasiveness by altering ZO‑1 expression

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