Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9.
E2F transcription factor 4
SUMOylation
hepatocellular carcinoma
lin‑9 DREAM MuvB core complex component
Journal
International journal of oncology
ISSN: 1791-2423
Titre abrégé: Int J Oncol
Pays: Greece
ID NLM: 9306042
Informations de publication
Date de publication:
Oct 2024
Oct 2024
Historique:
received:
20
12
2023
accepted:
14
06
2024
medline:
6
9
2024
pubmed:
6
9
2024
entrez:
6
9
2024
Statut:
ppublish
Résumé
SUMOylation plays a crucial role in numerous cellular biological and pathophysiological processes associated with human disease; however, the mechanisms regulating the genes involved in SUMOylation remain unclear. In the present study, E2F transcription factor 4 (E2F4) was identified as an E2F member related to hepatocellular carcinoma (HCC) progression by public database analysis. It was found that E2F4 promoted the proliferation and invasiveness of HCC cells via SUMOylation using Soft agar and Transwell migration assays. Mechanistically, it was demonstrated that E2F4 upregulated the transcript and protein expression levels of baculoviral IAP repeat containing 5, cell division cycle associated 8 and DNA topoisomerase II α using western blotting. Furthermore, the interaction between E2F4 with lin‑9 DREAM multi‑vulva class B core complex component (LIN9) was explored by co‑immunoprecipitation, immunofluorescence co‑localization and bimolecular fluorescence complementation assays. Moreover, it was demonstrated that E2F4 promoted the progression of HCC cells via LIN9. Rescue experiments revealed that LIN9 facilitated the SUMOylation and proliferation of HCC cells, which was prevented by knocking down E2F4 expression. In conclusion, the findings of the present study indicated that E2F4 plays a major role in the proliferation of HCC cells and may be a potential therapeutic target in the future.
Identifiants
pubmed: 39239750
doi: 10.3892/ijo.2024.5686
pii: 98
doi:
pii:
Substances chimiques
E2F4 Transcription Factor
0
E2F4 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM