Journal of Cancer Therapy

Volume 15, Issue 1 (January 2024)

ISSN Print: 2151-1934   ISSN Online: 2151-1942

Google-based Impact Factor: 0.30  Citations  h5-index & Ranking

Molecular Mechanism of KDM5B Development in Hepatocellular Carcinoma

HTML  XML Download Download as PDF (Size: 295KB)  PP. 1-12  
DOI: 10.4236/jct.2024.151001    47 Downloads   184 Views  
Author(s)

ABSTRACT

Objective: To investigate the mechanism of cell cyclin-dependent kinase (KDM5B), a key enzyme driving all cell cycle transitions, promoting HCC progression and metastasis. Methods: The expression of KDM5B in normal liver, HCC and its adjacent tissues was analyzed by RT-PCR and IHC. Lentivirus transfection method was used to construct stable cell lines with KDM5B overexpression and down-regulation, and the role of KDM5B in HCC migration and invasion was detected at cell level and animal level. Western blotting and Transwell experiments were performed to verify the effect of KDM5B and/or CCR2 inhibitors on HCC progression and metastasis by using liver orthotopic transplantation tumor model and immunofluorescence methods. Results: RT-PCR showed that the expression level of KDM5B in HCC was significantly higher than that in adjacent tissues, and the increase of KDM5B was relatively significant. Upregulation of KDM5B in nude mouse liver orthotopic transplantation tumor model can promote the incidence of lung metastasis and shorten the survival time of nude mice, whereas upregulation of KDM5B can reduce the incidence of lung metastasis and prolong the survival time of nude mice. Conclusion: This study clarified the expression of KDM5B in HCC and its function in promoting HCC migration, invasion and metastasis. The molecular mechanism of KDM5B promoting HCC metastasis was revealed, providing a potential therapeutic target for HCC.

Share and Cite:

Fu, S. and Guo, M. (2024) Molecular Mechanism of KDM5B Development in Hepatocellular Carcinoma. Journal of Cancer Therapy, 15, 1-12. doi: 10.4236/jct.2024.151001.

Cited by

No relevant information.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.