The Tumor Microenvironment-Dependent Transcription Factors AHR and HIF-1α Are Dispensable for Leukemogenesis in the Eµ-TCL1 Mouse Model of Chronic Lymphocytic Leukemia.
Susanne GonderAnne LargeotErnesto GargiuloSandrine PiersonIria Fernandez BotanaGiulia PaganoJérôme PaggettiEtienne MoussayPublished in: Cancers (2021)
Chronic lymphocytic leukemia (CLL) is the most frequent leukemia in the elderly and is characterized by the accumulation of mature B lymphocytes in peripheral blood and primary lymphoid organs. In order to proliferate, leukemic cells are highly dependent on complex interactions with their microenvironment in proliferative niches. Not only soluble factors and BCR stimulation are important for their survival and proliferation, but also the activation of transcription factors through different signaling pathways. The aryl hydrocarbon receptor (AHR) and hypoxia-inducible factor (HIF)-1α are two transcription factors crucial for cancer development, whose activities are dependent on tumor microenvironment conditions, such as the presence of metabolites from the tryptophan pathway and hypoxia, respectively. In this study, we addressed the potential role of AHR and HIF-1α in chronic lymphocytic leukemia (CLL) development in vivo. To this end, we crossed the CLL mouse model Eµ-TCL1 with the corresponding transcription factor-conditional knock-out mice to delete one or both transcription factors in CD19+ B cells only. Despite AHR and HIF-1α being activated in CLL cells, deletion of either or both of them had no impact on CLL progression or survival in vivo, suggesting that these transcription factors are not crucial for leukemogenesis in CLL.
Keyphrases
- chronic lymphocytic leukemia
- transcription factor
- mouse model
- induced apoptosis
- peripheral blood
- dna binding
- endothelial cells
- signaling pathway
- cell cycle arrest
- acute myeloid leukemia
- genome wide identification
- stem cells
- acute lymphoblastic leukemia
- oxidative stress
- endoplasmic reticulum stress
- free survival
- papillary thyroid
- type diabetes
- climate change
- cell death
- tyrosine kinase
- epithelial mesenchymal transition
- adipose tissue
- binding protein
- lymph node metastasis
- insulin resistance