Azathioprine is used to
suppress cells involved in autoimmune diseases.
Not exact matches
One factor keeping
cells in this immature state is the PTEN gene, which
suppresses a signalling pathway
involved in
cell growth.
Plakoglobin is a component of two important structures
involved in
cell - to -
cell adhesion, and the investigators found that
suppressing its expression caused CTC clusters to fall apart, reducing their metastatic potential, and also disrupted
cell - to -
cell contact between breast cancer
cells but not normal breast tissue.
The research team found that this non-coding RNA fragment maintains healthy
cells through two mechanisms: Firstly by regulating the levels of DIRAS3, one of its neigboring genes that is
involved in
cell replication; secondly by
suppressing a network of genes that prepare
cells to change their shape and prepare for metastasis.
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.
These factors work together to activate genes
involved in fashioning heart muscle
cells, while
suppressing genes characteristic of other
cell types.
Children with asthma have lower vitamin A levels than children without asthma, and the degree of vitamin A deficiency they exhibit is directly proportional to the severity of their asthma.37, 38 In
cell experiments, vitamin A eliminates the response of bronchial smooth muscle
cells to growth factors that characterizes the asthmatic reaction39 and
suppresses the activity of mast
cells, which are
involved in asthmatic or other reactions mediated by histamine or other inflammatory chemical messengers called leukotrienes.40 Consistent with studies in isolated
cells, vitamin A deficiency causes asthmatic bronchial hyper - reactivity in live rats.41