Prosapogenin A, a saponin from Chinese herb Veratrum nigrum (black false hellebore or Li Lu in Chinese herbalism), could inhibit cell growth and
promote cell apoptosis.
Not exact matches
Their antioxidant activity is known to inhibit
cell proliferation and invasion, and
promote apoptosis (
cell death) in various cancer
cells.
«We've long known that NF - kB
promotes cancer development by subverting
apoptosis, an internal safety mechanism that otherwise would cause cancer
cells to self - destruct,» says principal investigator Denis Guttridge, PhD, professor of molecular virology, immunology and medical genetics and of molecular and cellular biochemistry.
When it reaches the brain, Zika virus infects neuronal stem
cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it
promotes apoptosis, i.e. the early death of these neuronal
cells.
Rather, the group speculates that the transplanted
cells secreted protective neurotrophins, proteins that
promote cell survival by keeping neurons from inducing
apoptosis (programmed
cell death).
Gradual increase of p53 levels activates
apoptosis promoting protein Bak on the surface of the mitochondria making these
cells vulnerable to death.
Moreover; the PI3K / AKT pathway also can contribute to melanoma tumorigenesis through mutations or loss in PTEN and dysregulation in expression of AKT, which positively regulates the G1 / S phase progression in
cell cycle, suppresses
apoptosis and
promotes cellular survival.
Binding of PD - L1 to the co-stimulatory receptor on T
cells, PD - 1,
promotes inactivation and
apoptosis of activated anti-tumor T
cells.
Tumor - associated B7 - H1
promotes T -
cell apoptosis: a potential mechanism of immune evasion.
Stem
cells affect the infarcted myocardium via neovascularization, reduction of
apoptosis and paracrine effect, they are able to increase myocardial perfusion, inhibit synthesis of pro-inflammatory cytokines (IL6 and TNFα) and
promote expression of anti-inflammatory cytokines (IL10) minimizing the necrosis damage caused by local inflammatory reaction.
Activation of ERK1 / 2 triggers G2 checkpoint which is considered protective from radiation - induced
cell death [8, 9], while activated AKT is known to
promote DNA repair and inhibition of
apoptosis induction [10].
Independent of MMP activity, TIMP - 1 can
promote growth and inhibit
apoptosis through various pathways, including P13K and PKA [9] and, furthermore, TIMP - 1 is able to provide β
cell - specific pro-survival effects [5, 6, 10].
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.
Notably, genes thought to induce and
promote apoptosis through the intrinsic mitochondrial apoptotic pathway, such as KLF10 [32], were not altered in differentiated
cells or in treated versus untreated
cells.
Melanoma Differentiation Associated Gene - 7 / Interleukin - 24
Promotes Tumor
Cell - Specific
Apoptosis through Both Secretory and Nonsecretory Pathways
Finally the soy isoflavone genistein reduces DNA synthesis in the brain, reducing the birth of new brain
cells and
promoting apoptosis and
cell death.
Estradiol
promotes the onco (cancer) gene, Bcl - 2, while progesterone
promotes the protective gene known as p53 which slows
cell apoptosis.
It
promotes tumor
cell proliferation and resistance to
apoptosis (programmed
cell death after a certain number of
cell divisions, a good thing when it comes to cancer
cells).
A review of human, animal and test - tube studies, published in 2016 in Critical Reviews in Food Science and Nutrition, found that broccoli glucosinolates
promote apoptosis, or cancer
cell death.
In cancer therapy, melatonin counteracts chemotherapy toxicity, by acting as an anti-oxidant agent, and
promotes apoptosis (programmed
cell death) of cancer
cells, thus enhancing the toxicity of chemotherapy.
RemedyLink Ellagic Acid contains a blend of USP grade ellagic acid and specific herbs which offer many health benefits, some of which include inhibiting fungi and yeast growth, killing bacteria,
promoting the
apoptosis of certain
cells, and more.
In a study published this year in Current Drug Targets, a combination of tocotrienols and quercetin induced senescence and
promoted apoptosis in many different types of cancer
cells, while delaying senescence in healthy
cells and rejuvenating formerly healthy senescent
cells.
Instead, they turned on genes that
promote the death of cancer
cells (known as
apoptosis) and the growth of healthy, normal
cells!
Studies have shown gamma - tocotrienol selectively targets cancer
cells, triggering cellular senescence and
promoting apoptosis — a type of programmed
cell suicide.
Pomegranate's antioxidant activity is known to inhibit
cell proliferation and invasion, and
promote apoptosis (
cell death) in various cancer
cells.
Their antioxidant activity is known to inhibit
cell proliferation and invasion, and
promote apoptosis (
cell death) in various cancer
cells.
Included in those is disrupting cancer
cell replication, targeting and disrupting cancer stem
cell development, and
promoting cancer
cell apoptosis (
cell destruction)(6).
It is hypothesized that chronic ingestion of a high - carbohydrate diet
promotes obesity and increases the demand on β -
cells for insulin secretion, thereby predisposing individuals to hyperinsulinemia,
apoptosis, β -
cell failure, and development of type 2 diabetes (21).
Essential oils can and do still benefit these issues - as they can help the body to remove inflammation, support the body systems in repair, improve immune system function, relieve stress and discomfort, support the surrounding muscle and tissue structures,
promote death of abnormal
cells (
apoptosis of tumor
cells), provide antibacterial and antiviral actions, and more.