lncRNA ZNF667-AS1 suppresses hepatitis B virus-related hepatocellular carcinoma by regulating miR-210-3p to upregulate CPEB2.
- 1Department of Infectious Diseases, Rudong People's Hospital, No. 2, Jianghai West Road, Chengzhong Subdistrict, Rudong County, Nantong, 226400, China.
- 2Department of Infectious Diseases, Rudong People's Hospital, No. 2, Jianghai West Road, Chengzhong Subdistrict, Rudong County, Nantong, 226400, China. [email protected].
Abstract
Background
To explore the biological functions, clinical significance, and regulatory mechanism of long non-coding RNA (lncRNA) ZNF667-AS1 in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).Methods
One hundred and seven patients with HBV-related HCC, one hundred and five patients with chronic hepatitis B (CHB) and one hundred and five healthy controls were enrolled in this study. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of ZNF667-AS1, miR-210-3p, CPEB2. The association between ZNF667-AS1 expression and clinical characteristics of patients were analyzed, and receiver operating characteristic (ROC) curve analysis was performed to evaluate its diagnostic value. Bioinformatics prediction and dual-luciferase reporter assays were conducted to verify the targeted associations between ZNF667-AS1 and miR-210-3p, as well as between miR-210-3p and CPEB2. Cell Counting Kit-8 (CCK-8) and Transwell assays were applied to assess the biological functions of HCC cells after cell transfection.Results
The expression levels of ZNF667-AS1 and CPEB2 were significantly downregulated in tissue samples from patients with HBV-related HCC and in HBV-associated HCC cell lines. ROC curve analysis showed the area under the curve (AUC) of ZNF667-AS1 for diagnosing HBV-related HCC from CHB reached 0.841. miR-210-3p was validated as a direct target of ZNF667-AS1, and a significant negative correlation was observed between their expression levels. Overexpression of ZNF667-AS1 inhibited the proliferation, migration, and invasion of HCC cells, whereas this inhibitory effect was reversed by transfection with miR-210-3p mimic.Conclusions
LncRNA ZNF667-AS1 is downregulated in HBV-related HCC and exerts in vitro tumor‑suppressive effects by targeting miR-210-3p to upregulate CPEB2 expression, thus providing a potential auxiliary biomarker for HBV-related HCC diagnosis and a novel regulatory axis for understanding disease pathogenesis.
Related
- A hybrid deep learning and ensemble approach for accurate prediction of hepatocellular carcinoma from sequence variants of hepatitis B virus (HBV) X gene
- Inhibition of Bone Morphogenetic Protein 2 Suppresses the Stemness Maintenance of Cancer Stem Cells in Hepatocellular Carcinoma via the MAPK/ERK Pathway [Retraction].
- MYC Suppresses Mitochondrial Function in Hepatocellular Carcinoma through NRF1-Driven Receptor-Mediated Mitophagy
- Identification of hepatitis B virus-associated membrane proteins as prognostic biomarkers for hepatocellular carcinoma based on retrospective analysis of integrated membrane proteomics
- Superior Efficacy of Besifovir in Reducing Hepatocellular Carcinoma Risk Compared to Tenofovir in Chronic Hepatitis B Patients: A Nationwide Cohort Study
BibTeX
@article{cong2026lncrna,
title = {{lncRNA ZNF667-AS1 suppresses hepatitis B virus-related hepatocellular carcinoma by regulating miR-210-3p to upregulate CPEB2.}},
author = {Huimin Cong and Guobing Zhu and Yingzhou Xu and Linlin Wu and Hongfang Gu and Chunyan Dai},
journal = {Virology journal},
year = {2026},
month = jul,
doi = {10.1186/s12985-026-03260-9},
url = {https://europepmc.org/article/MED/42919296},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - lncRNA ZNF667-AS1 suppresses hepatitis B virus-related hepatocellular carcinoma by regulating miR-210-3p to upregulate CPEB2.
AU - Huimin Cong
AU - Guobing Zhu
AU - Yingzhou Xu
AU - Linlin Wu
AU - Hongfang Gu
AU - Chunyan Dai
PY - 2026
DA - 2026/07/01
JO - Virology journal
DO - 10.1186/s12985-026-03260-9
UR - https://europepmc.org/article/MED/42919296
AB - Background To explore the biological functions, clinical significance, and regulatory mechanism of long non-coding RNA (lncRNA) ZNF667-AS1 in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).Methods One hundred and seven patients with HBV-related HCC, one hundred and five patients with chronic hepatitis B (CHB) and one hundred and five healthy controls were enrolled in this study. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of ZNF667-AS1, miR-210-3p, CPEB2. The association between ZNF667-AS1 expression and clinical characteristics of patients were analyzed, and receiver operating characteristic (ROC) curve analysis was performed to evaluate its diagnostic value. Bioinformatics prediction and dual-luciferase reporter assays were conducted to verify the targeted associations between ZNF667-AS1 and miR-210-3p, as well as between miR-210-3p and CPEB2. Cell Counting Kit-8 (CCK-8) and Transwell assays were applied to assess the biological functions of HCC cells after cell transfection.Results The expression levels of ZNF667-AS1 and CPEB2 were significantly downregulated in tissue samples from patients with HBV-related HCC and in HBV-associated HCC cell lines. ROC curve analysis showed the area under the curve (AUC) of ZNF667-AS1 for diagnosing HBV-related HCC from CHB reached 0.841. miR-210-3p was validated as a direct target of ZNF667-AS1, and a significant negative correlation was observed between their expression levels. Overexpression of ZNF667-AS1 inhibited the proliferation, migration, and invasion of HCC cells, whereas this inhibitory effect was reversed by transfection with miR-210-3p mimic.Conclusions LncRNA ZNF667-AS1 is downregulated in HBV-related HCC and exerts in vitro tumor‑suppressive effects by targeting miR-210-3p to upregulate CPEB2 expression, thus providing a potential auxiliary biomarker for HBV-related HCC diagnosis and a novel regulatory axis for understanding disease pathogenesis.
SN - 1743-422X
ER -