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Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9

  • Authors:
    • Zhenwei Ma
    • Qilan Li
    • Wenjing Wang
    • Zhengdong Deng
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    Affiliations: Department of Hepatobiliary and Pancreatic Surgery, Tianyou Hospital, Wuhan University of Science and Technology, Wuhan, Hubei 430064, P.R. China, Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China, Department of Pediatric Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
    Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 98
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    Published online on: September 2, 2024
       https://doi.org/10.3892/ijo.2024.5686
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Ma Z, Li Q, Wang W and Deng Z: Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9. Int J Oncol 65: 98, 2024.
APA
Ma, Z., Li, Q., Wang, W., & Deng, Z. (2024). Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9. International Journal of Oncology, 65, 98. https://doi.org/10.3892/ijo.2024.5686
MLA
Ma, Z., Li, Q., Wang, W., Deng, Z."Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9". International Journal of Oncology 65.4 (2024): 98.
Chicago
Ma, Z., Li, Q., Wang, W., Deng, Z."Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9". International Journal of Oncology 65, no. 4 (2024): 98. https://doi.org/10.3892/ijo.2024.5686
Copy and paste a formatted citation
x
Spandidos Publications style
Ma Z, Li Q, Wang W and Deng Z: Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9. Int J Oncol 65: 98, 2024.
APA
Ma, Z., Li, Q., Wang, W., & Deng, Z. (2024). Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9. International Journal of Oncology, 65, 98. https://doi.org/10.3892/ijo.2024.5686
MLA
Ma, Z., Li, Q., Wang, W., Deng, Z."Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9". International Journal of Oncology 65.4 (2024): 98.
Chicago
Ma, Z., Li, Q., Wang, W., Deng, Z."Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9". International Journal of Oncology 65, no. 4 (2024): 98. https://doi.org/10.3892/ijo.2024.5686
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