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.
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