We study the signal transduction
pathways regulating cell growth and proliferation, with an emphasis on kinase enzymes.
Not exact matches
The publication, «Androgens
Regulate Prostate Cancer
Cell Growth via an AMPK - PGC - 1α - Mediated Metabolic Switch,» featured online in Oncogene, illuminates a known metabolic
pathway as a potential novel therapeutic target.
Her work described the regulatory link between the metabolic enzyme ATP - citrate lyase and histone acetylation levels in mammalian
cells, and established that glucose utilization in the hexosamine biosynthetic
pathway regulates growth factor receptor signaling.
His lab studies a particular signaling
pathway, the RAS / RAF / MEK / ERK
pathway, which
regulates cell growth and survival in several cancers.
One of the key metabolic alterations that takes place during EMT is that of the epidermal
growth factor receptor (EGFR) which is a
pathway that
regulates growth, survival, proliferation, and differentiation in mammalian
cells.
University of California, Berkeley researchers have now found a promising new drug target within that
pathway that is appealing, in part, because it appears to control production of only a few percent of the body's many proteins, those critical to
regulating the
growth and proliferation of
cells.
Actually, almost all signalling
pathways that affect
cell growth and proliferation directly
regulate rRNA synthesis, their downstream effectors converging at the Pol I transcription machinery.
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.
The
pathways that connect expression of stem
cell surface glycoconjugates such as the TRA -1-60 / GCTM - 2 antigen, receptors, and
growth factors in human and even mouse ES
cells with the transcriptional networks that
regulate pluripotency remain unclear.
Pterostilbene limits the expression of the mTOR signaling
pathway, which helps to
regulate the
growth, survival and proliferation of
cells.
mTOR is a biological
pathway in the body which plays an important role in
regulating cell growth and proliferation that may also have an influence over cancer
growth (6).