Open Access

ARTICLE

Identification of key long noncoding RNAs and their biological functions in hepatocellular carcinoma

FEI CHEN^1,2, LIANG WANG^3,*, YUHONG LI^1,2,*

1 Medical College, Soochow University, Suzhou, 215006, China
2 Department of Ultrasound, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, China
3 Department of General Hepatobiliary Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, China

* Corresponding Authors: LIANG WANG. Email: ; YUHONG LI. Email:

(This article belongs to the Special Issue: Noncoding RNAs & Associated Human Diseases)

BIOCELL 2022, 46(7), 1687-1696. https://doi.org/10.32604/biocell.2022.018078

Received 28 June 2021; Accepted 18 August 2021; Issue published 17 March 2022

Abstract

Long noncoding RNAs (lncRNAs) are vital regulators in tumorigenesis and metastasis. However, the pathological role of lncRNAs in hepatocellular carcinoma (HCC) is still unclear. In this study, we filtered out three lncRNAs from The Cancer Genome Atlas (TCGA) data that were screened for basic expression and clinical research. We selected lncRNA-NEAT1 for further study to explore its function in HCC progression and its regulatory mechanism. We identified three differentially expressed lncRNAs (DElncRNAs) in tumor and adjacent normal tissues from the TCGA library using data mining methods: lncRNA-NEAT1, lncRNA-MAGI2-AS3 and lncRNA-HCG11. Their basic expression levels were detected by qPCR. Then, we selected lncRNA-NEAT1 as a potentially important lncRNA to verity its biological function and mechanism in HCC cell lines. lncRNA-NEAT1, lncRNA-MAGI2-AS3 and lncRNA-HCG11 were overexpressed in liver cancer tissues and cell lines. We found that silencing NEAT1 in vitro can inhibit the proliferation of HuH-7 and Li-7 cells, inhibit cell migration, and induce apoptosis as well as significantly increase the level of miR-16-5p. We also confirmed that miR-16-5p has a significant correlation with Bcl-2. When NEAT1 is silenced, the expression of Bcl-2 decreases. Inhibiting miR-16-5p can restore Bcl-2 to its original level. We conclude that miR-16-5p1/lncRNA NEAT1 plays a crucial role in regulating the delivery of Bcl-2 in HCC. Overall, the miR-16-5p/lncRNA-NEAT1/Bcl-2 signaling axis may be a promising target for HCC treatment.

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Keywords

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