E2F2 modulates cell adhesion through the transcriptional regulation of PECAM1 in multiple myeloma
E2F2 modulates cell adhesion through the transcriptional regulation of PECAM1 in multiple myeloma
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DOI：
10.1111/bjh.18958
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发表时间：
2023-06-26
影响因子：
6.5
通讯作者：
Zheng，Yongjiang
中科院分区：
文献类型：
--
作者：
Chen，Shu-Na;Mai，Zhi-Ying;Zheng，Yongjiang
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 thePECAM1promoter to suppress its transcriptional activity. TheE2F2‐knockdown‐mediated promotion of cell adhesion was significantly reversed by the repression ofPECAM1expression. Finally, we observed that silencingE2F2significantly 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.
