Positive selection on
apoptosis related genes.
Positive selection on
apoptosis related genes Fonseca, R. R., C. Kosiol, T. Vinař, A. Siepel et al. 2010.
Not exact matches
b. Creating synthetic receptors or signals of cancer, i.e. when cancer
related miRNA is activated, you have it also activate a synthetic
gene or protein, that is expressed on the membrane surface to activate
apoptosis.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and
apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is
related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent
gene expression program.
Approximately 50 % of PTCL are unclassifiable and categorized as PTCL, not otherwise specified (PTCL - NOS).1 Using
gene expression profiling, PTCL - NOS lymphocytes can be distinguished from normal T lymphocytes, with deregulation of
genes involved in
apoptosis, proliferation, cell adhesion, and transcription regulation.2 Two subgroups of PTCL - NOS have been identified, which are characterized by high expression of either GATA3 or TBX21 / T - bet transcription factors and downstream target
genes.3 However, actionable biomarkers closely
related to the pathogenic mechanism need to be further investigated and may become potential therapeutic targets of PTCL - NOS. 4, 5
These features were
related to a modified
gene expression pattern in adult male testes, showing an altered
gene expression in
genes involved in DNA repair and
apoptosis that was confirmed by TUNEL assay.
3Kang et al., H3N2 Canine Influenza Virus Causes Severe Morbidity in Dogs with Induction of
Genes Related to Inflammation and
Apoptosis, Veterinary Research 2013,44:92.