E2F2 modulates cell adhesion through the transcriptional regulation of PECAM1 in multiple myeloma

Shu Na Chen, Zhi Ying Mai, Jun Na Mai, Weiyao Liang, Zhao Xia Dong, Fei er Ju, Sze Hoi Chan, Zhigang Fang, Yichuan Xu, Orit Uziel, Chengwei He, Xing Ding Zhang*, Yongjiang Zheng*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Multiple myeloma (MM) is the second most common haematological malignancy. Despite the development of new drugs and treatments in recent years, the therapeutic outcomes of patients are not satisfactory. It is necessary to further investigate the molecular mechanism underlying MM progression. Herein, we found that high E2F2 expression was correlated with poor overall survival and advanced clinical stages in MM patients. Gain- and loss-of-function studies showed that E2F2 inhibited cell adhesion and consequently activated cell epithelial-to-mesenchymal transition (EMT) and migration. Further experiments revealed that E2F2 interacted with the PECAM1 promoter to suppress its transcriptional activity. The E2F2-knockdown-mediated promotion of cell adhesion was significantly reversed by the repression of PECAM1 expression. Finally, we observed that silencing E2F2 significantly inhibited viability and tumour progression in MM cell models and xenograft mouse models respectively. This study demonstrates that E2F2 plays a vital role as a tumour accelerator by inhibiting PECAM1-dependent cell adhesion and accelerating MM cell proliferation. Therefore, E2F2 may serve as a potential independent prognostic marker and therapeutic target for MM.

Original languageEnglish
Pages (from-to)840-855
Number of pages16
JournalBritish Journal of Haematology
Issue number4
StatePublished - Aug 2023


  • E2F2
  • PECAM1
  • cell adhesion
  • multiple myeloma


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