CircMYBL2 facilitates hepatocellular carcinoma progression by regulating E2F1 expression.


Journal

Oncology research
ISSN: 1555-3906
Titre abrégé: Oncol Res
Pays: United States
ID NLM: 9208097

Informations de publication

Date de publication:
2024
Historique:
received: 08 11 2023
accepted: 28 12 2023
medline: 3 6 2024
pubmed: 3 6 2024
entrez: 3 6 2024
Statut: epublish

Résumé

Circular RNAs (circRNAs) have been recognized as pivotal regulators in tumorigenesis, yet the biological functions as well as molecular mechanisms of the majority of circRNAs in hepatocellular carcinoma (HCC) remain elusive. We sought to unveil the expression profile and biological role of circMYBL2 in HCC. Initial microarray analyses were conducted to probe the expression profile of circMYBL2 in HCC cells, and qRT‒PCR analysis was then performed in HCC cell lines and tissues, revealing significant upregulation of circMYBL2. Subsequent experiments were conducted to evaluate the biological function of circMYBL2 in HCC progression. Furthermore, bioinformatics analysis, qRT‒PCR analysis, luciferase reporter assays, and western blot analysis were employed to investigate the interplay among circMYBL2, miR-1205, and E2F1. CircMYBL2 was found to exhibit marked upregulation in tumor tissues as well as HCC cell lines. Elevated expression of circMYBL2 increased the proliferation and migration of HCC cells, whereas circMYBL2 knockdown elicited contrasting effects. Mechanistically, our results indicated that circMYBL2 promoted E2F1 expression and facilitated HCC progression by sponging miR-1205. Our findings revealed that circMYBL2 contributed to HCC progression through the circMYBL2/miR-1205/E2F1 axis, suggesting the potential of circMYBL2 as a novel target for HCC treatment or a prognostic biomarker for HCC.

Identifiants

pubmed: 38827325
doi: 10.32604/or.2024.047524
pii: 47524
pmc: PMC11136682
doi:

Substances chimiques

E2F1 Transcription Factor 0
RNA, Circular 0
E2F1 protein, human 0
MicroRNAs 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1129-1139

Informations de copyright

© 2024 Yi et al.

Déclaration de conflit d'intérêts

The authors declare that they have no conflicts of interest to report regarding the present study.

Auteurs

Junzhe Yi (J)

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Binbin Li (B)

Department of Medical Oncology, The Third People's Hospital of Yongzhou, Yongzhou, 425000, China.

Xiaomin Yin (X)

Department of Radiotherapy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, China.

Lingrui Liu (L)

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Cailu Song (C)

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Ying Zhao (Y)

Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.

Manbo Cai (M)

Department of Radiotherapy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, China.

Hailin Tang (H)

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Dong Chen (D)

Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.

Ning Lyu (N)

State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

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Classifications MeSH