Dataset Information

Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma.

ABSTRACT:

Background

Hepatocellular carcinoma (HCC) is a malignant disease with a high mortality among primary HCC patients worldwide. Lots of studies have shown that lncRNAs are known as the biomarkers in diagnosis, treatment and prognosis of hepatocellular carcinoma. Therefore, clarifying the detailed function and mechanism of the lncRNA in the HCC progressing seems particularly important.

Methods

The TCGA and GEO database and RT-qPCR were used to analyse the expression of TRIM52-AS1 in HCC tissues and cell lines. Clinical data were collected to further analyze the correlation between indicators of clinical samples and the expression of TRIM52-AS1. CCK-8, plate clone and transwell assays were employed to evaluate the role of TRIM52-AS1 on cell proliferation, migration and invasion. Then, bioinformatics prediction, luciferase reporter, RNA immunoprecipitation (RIP), and RT-qPCR were employed to analyze the direct interaction among TRIM52-AS1, miR-218-5p and ROBO1. Additionally, the rescue function assays were used to verify that miR-218-5p/ROBO1 was the function downstream of TRIM52-AS1.

Results

TRIM52-AS1 was overexpressed in HCC according to the TCGA database and RT-qPCR assay. The expression of TRIM52-AS1 was higher in the metastatic foci compared with primary tumor according to the GEO database. Additionally, TRIM52-AS1 knockdown inhibited the proliferation and metastasis of HCC cells. TRIM52-AS1 could act as competitive endogenous RNA to regulate ROBO1 through miR-218-5p, then promoted the HCC cell progression.

Conclusion

TRIM52-AS1 is overexpressed in HCC and can promote the proliferation and metastasis of HCC cells through miR-218-5p/ROBO1 axis, then drives the HCC cell progression.

SUBMITTER: Liu Y

PROVIDER: S-EPMC7837577 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Publications

Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma.

Liu Yuanjun Y Wu Yakun Y Liu Shuang S Dai Yi Y

Cancer management and research 20210122

<h4>Background</h4>Hepatocellular carcinoma (HCC) is a malignant disease with a high mortality among primary HCC patients worldwide. Lots of studies have shown that lncRNAs are known as the biomarkers in diagnosis, treatment and prognosis of hepatocellular carcinoma. Therefore, clarifying the detailed function and mechanism of the lncRNA in the HCC progressing seems particularly important.<h4>Methods</h4>The TCGA and GEO database and RT-qPCR were used to analyse the expression of TRIM52-AS1 in H ...[more]

PMID: 33519234

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Project description:BackgroundAccumulating evidence has highlighted the potential role of long non-coding RNAs (lncRNAs) in the biological behaviors of hepatocellular carcinoma (HCC). Here, we elucidated the function and possible molecular mechanisms of the effect of lncRNA-AGAP2-AS1 on the biological behaviors of HCC.MethodsEdU, Transwell and flow cytometry were used to determine proliferation, migration, invasion and apoptosis of HCC cells in vitro. The subcutaneous tumor model and lung metastasis mouse model in nude mice was established to detect tumor growth and metastasis of HCC in vivo. The direct binding of miR-16-5p to 3'UTR of ANXA11 was confirmed by luciferase reporter assay. The expression of AGAP2-AS1 and miR-16-5p in HCC specimens and cell lines were detected by real-time PCR. The correlation among AGAP2-AS1 and miR-16-5p were disclosed by a dual-luciferase reporter assay, RIP assay and biotin pull-down assay.ResultsHere, we demonstrated that AGAP2-AS1 expression was up-regulated in HCC tissues and cell lines, especially in metastatic and recurrent cases. Gain- and loss-of-function experiments indicated that AGAP2-AS1 promoted cell proliferation, migration, invasion, EMT progression and inhibited apoptosis of HCC cells in vitro and in vivo. Further studies demonstrated that AGAP2-AS1 could function as a competing endogenous RNA (ceRNA) by sponging miR-16-5p in HCC cells. Functionally, gain- and loss-of-function studies showed that miR-16-5p promoted HCC progression and alteration of miR-16-5p abolished the promotive effects of AGAP2-AS1 on HCC cells. Moreover, ANXA11 was identified as direct downstream targets of miR-16-5p in HCC cells, and mediated the functional effects of miR-16-5p and AGAP2-AS1 in HCC, resulting in AKT signaling activation. Clinically, AGAP2-AS1 and miR-16-5p expression were markedly correlated with adverse clinical features and poor prognosis of HCC patients. We showed that hypoxia was responsible for the overexpression of AGAP2-AS1 in HCC. And the promoting effects of hypoxia on metastasis and EMT of HCC cells were reversed by AGAP2-AS1 knockdown.ConclusionsTaken together, this research supports the first evidence that AGAP2-AS1 plays an oncogenic role in HCC via AGAP2-AS1/miR-16-5p/ANXA11/AKT axis pathway and represents a promising therapeutic strategy for HCC patients.

Dataset Information

Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma.

Background

Methods

Results

Conclusion

Publications

Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma.

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