期刊
ONCOTARGET
卷 7, 期 24, 页码 36854-36864出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9210
关键词
classical Hodgkin lymphoma (cHL); TCF3/E2A; cell death
资金
- Deutsche Krebshilfe e.V. [107547]
- National Natural Science Foundation of China [81101788, 81572857, 81201867]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars by the State Education Ministry
Although Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) derived from germinal or post germinal B cells, they have lost the B cell phenotype in the process of lymphomagenesis. The phenomenon can be at least partially explained by repression of B-cell-specific transcription factors including TCF3, early B-cell factor 1 (EBF1), SPI1/PU.1, and FOXO1, which are down-regulated by genetic and epigenetic mechanisms. The unique phenotype has been suspected to be advantageous for survival of HRS cells. Ectopic expression of some of these transcription factors (EBF1, PU.1, FOXO1) indeed impaired survival of cHL cells. Here we show that forced expression of TCF3 causes cell death and cell cycle arrest in cHL cell lines. Mechanistically, TCF3 overexpression modulated expression of multiple pro-apoptotic genes including BIK, APAF1, FASLG, BOK, and TNFRSF10A/DR4. We conclude that TCF3 inactivation contributes not only to extinguishing of B cell phenotype but also to cHL oncogenesis.
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