Results 61 to 70 of about 369,993 (297)

The anticancer effect of the HDAC inhibitor belinostat is enhanced by inhibitors of Bcl‐xL or Mcl‐1 in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
The pan‐HDAC inhibitor belinostat increases the expression of the pro‐apoptotic proteins Bim, Puma, and Noxa and induces apoptosis in ovarian cancer cell lines and patient‐derived tumor organoids when used at high concentrations. Moreover, inhibiting the anti‐apoptotic proteins Bcl‐xL or Mcl‐1 sensitizes these preclinical models to the cytotoxic effect
Cécilia Thomine   +10 more
wiley   +1 more source

IMMUNOHISTOCHEMICAL EXPRESSION OF p53 AND BCL-2 PROTEINS IN ADVANCED ESOPHAGEAL CANCER PATIENTS [PDF]

open access: yesActa Medica Iranica, 2005
The current challenges in the management of esophageal cancer are to obtain a better understanding of underlying molecular alterations to provide new treatment options. We studied the p53 and Bcl-2 protein expression in esophageal carcinomas to correlate
S. Arbabi Bidgoli   +4 more
doaj   +2 more sources

MDA-7/IL-24 induces Bcl-2 denitrosylation and ubiquitin-degradation involved in cancer cell apoptosis.

open access: yesPLoS ONE, 2012
MDA-7/IL-24 was involved in the specific cancer apoptosis through suppression of Bcl-2 expression, which is a key apoptosis regulatory protein of the mitochondrial death pathway. However, the underlying mechanisms of this regulation are unclear.
Hui Tian   +8 more
doaj   +1 more source

BCL-W has a fundamental role in B cell survival and lymphomagenesis. [PDF]

open access: yes, 2017
Compromised apoptotic signaling is a prerequisite for tumorigenesis. The design of effective therapies for cancer treatment depends on a comprehensive understanding of the mechanisms that govern cell survival.
Annette S. Kim   +14 more
core   +2 more sources

Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis

open access: yesMolecular Oncology, EarlyView.
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach   +8 more
wiley   +1 more source

Somatic hypermutation of IGVH genes and aberrant somatic hypermutation in follicular lymphoma without BCL-2 gene rearrangement and expression

open access: yesHaematologica, 2008
Background Follicular lymphoma is characterized by the t(14;18) translocation resulting in constitutive expression of BCL-2 protein; however approximately 10–15% of follicular lymphomas do not express BCL-2 protein, and a small fraction of these cases ...
Éva Gagyi   +9 more
doaj   +1 more source

The Effect of T69E-mimicked Phosphorylation on the Interaction Between Bcl-2 and Nur77

open access: yesChinese Journal of Magnetic Resonance, 2022
Bcl-2 mainly executes anti-apoptotic function in the Bcl-2 family. Nuclear orphan receptor Nur77 can be translocated from nucleus to mitochondria, then interact with Bcl-2 to reverse the function of Bcl-2 from a cell protector to a cell killer, thereby ...
Qian XU   +5 more
doaj   +1 more source

The phosphorylation status and anti-apoptotic activity of Bcl-2 are regulated by ERK and protein phosphatase 2A on the mitochondria [PDF]

open access: yes, 2004
Bcl-2 protein play important roles in the regulation of apoptosis. We previously reported that the phosphorylation of Bcl-2 was augmented by treatment with protein phosphatase 2A (PP2A) inhibitor; however, the kinase responsible for Bcl-2 phosphorylation
Osada, Hiroyuki   +2 more
core   +1 more source

Adenosine A3 receptor antagonists as anti‐tumor treatment in human prostate cancer: an in vitro study

open access: yesFEBS Open Bio, EarlyView.
The A3 adenosine receptors (A3ARs) are overexpressed in prostate cancer. AR 292 and AR 357, as A3AR antagonists, are capable of blocking proliferation, modulating the expression of drug transporter genes involved in chemoresistance, ferroptosis, and the hypoxia response, and inducing cell death.
Maria Beatrice Morelli   +15 more
wiley   +1 more source

Soman induces endoplasmic reticulum stress and apoptosis of cerebral organoids via the GRP78‐ATF6‐CHOP signaling pathway

open access: yesFEBS Open Bio, EarlyView.
Cerebral organoids were employed as a novel model to explore the neurotoxicity of soman. Soman inhibited acetylcholinesterase activity, increased cell apoptosis and upregulated endoplasmic reticulum (ER) stress markers glucose‐regulated protein 78 (GRP78), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP).
Yue Wei   +7 more
wiley   +1 more source

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