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Role of hsa_circ_0066966 in proliferation and migration of hepatitis B virus-related liver cancer cells.

ABSTRACT: A large proportion of liver cancer cases is caused by hepatitis B virus (HBV) infection. In recent years, an increasing number of reports have indicated that circular RNAs (circRNAs) exert regulatory effects in cancer development, whereas the role of circRNAs in HBV-positive liver cancer requires further investigation. In the present study, abnormally expressed circRNAs were identified in HBV-positive liver cancer cells through microarray analysis. A total of 1,493 differentially expressed circRNAs [absolute fold-change (FC) ≥2] in HBV-positive liver cancer cells were detected, of which 171 were upregulated and 1,322 were downregulated. Subsequently, Gene Ontology enrichment analysis indicated that the genes of dysregulated circRNAs were mainly involved in regulating Sertoli cell differentiation and development, as well as telomeric DNA binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that most of these genes were enriched in cancer-related signaling pathways, including the MAPK and Hippo signaling pathways. Next, the expression levels of the top-10 dysregulated circRNAs were verified in HBV-positive liver cancer cells through reverse transcription-quantitative PCR. Among them, hsa_circ_0066966 had the highest absolute Log₂FC value and was abnormally increased in HBV-positive liver cancer cells. Functional experiments further verified that knockdown of hsa_circ_0066966 had a significant inhibitory effect on the proliferation and migration of HBV-positive liver cancer cells. By contrast, overexpression of hsa_circ_0066966 in HBV-negative liver cancer cells resulted in the opposite effect. In conclusion, in the present study, comprehensive circRNA profiling in HBV-positive liver cancer cells indicated that hsa_circ_0066966 may regulate the progression of HBV-positive liver cancer.

SUBMITTER: Yuan Y

PROVIDER: S-EPMC8674973 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Interleukin-7 receptor (IL-7R) is involved in the abnormal function of solid tumors, but the role and regulatory mechanisms of IL-7R in HBV-related hepatocellular carcinoma (HCC) are still unclear.Gene and protein expression levels of IL-7R were examined in hepatoma cells transfected with hepatitis B virus (HBV) plasmids and in hepatoma cells transfected with the multifunctional nonstructural protein X (HBX). The expression of HBX and IL-7R was measured by immunohistochemical analysis in HBV-related HCC tissues. The role of NF-?B and Notch1 pathways in HBX-mediated expression of IL-7R in hepatoma cells was examined. Activation of IL-7R downstream of intracellular signaling proteins AKT, JNK, STAT5, and the associated molecules CyclinD1 and matrix metalloproteinase-9 (MMP)-9, was assessed in HBX-positive cells with or without treatment with IL-7R short hairpin RNA (shRNA). Additionally, the role of IL-7R in HBX-mediated proliferation and migration of hepatoma cells was investigated.The expression of IL-7R was increased in hepatoma cells transfected with HBV plasmids; HBX was responsible for the HBV-mediated upregulation of IL-7R. Compared to adjacent tissues, the expression of HBX and IL-7R was increased in HBV-related HCC tissues. Additionally, the relative expression levels of HBX were associated with IL-7R in HBV-related HCC tissues. The activation of NF-?B pathways and expression of Notch1 were increased in hepatoma cells transfected with HBX, and inhibition of NF-?B and Notch1 pathways significantly decreased HBX-mediated expression of IL-7R. The activation of AKT and JNK and the expression of CyclinD1 and MMP-9 were increased in HBX-positive cells. When cells were treated with IL-7R shRNA, the activation of AKT and JNK, as well as the expression of CyclinD1 and MMP-9, were significantly inhibited. Additionally, IL-7R was responsible for HBX-induced proliferation and migration ability of hepatoma cells.Our data demonstrate that HBX can upregulate IL-7R via NF-?B and Notch1 pathways to facilitate the activation of intracellular pathways and expression of associated molecules, and contribute to proliferation and migration of hepatoma cells.

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Role of hsa_circ_0066966 in proliferation and migration of hepatitis B virus-related liver cancer cells.

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