Results 141 to 150 of about 304,002 (266)

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

open access: yesMolecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy   +12 more
wiley   +1 more source

Integration of single‐cell and bulk RNA‐sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer

open access: yesMolecular Oncology, EarlyView.
Prostate cancer is a leading malignancy with significant clinical heterogeneity in men. An 11‐gene signature derived from dysregulated epithelial cell markers effectively predicted biochemical recurrence‐free survival in patients who underwent radical surgery or radiotherapy.
Zhuofan Mou, Lorna W. Harries
wiley   +1 more source

Editorial: Immunometabolism of T cells in skin infection, autoimmunity and cancer biology

open access: yesFrontiers in Immunology, 2023
Lu Peng   +4 more
doaj   +1 more source

Numerical status of CD4+CD25+FoxP3+ and CD8+CD28- regulatory T cells in multiple sclerosis [PDF]

open access: yesIranian Journal of Basic Medical Sciences, 2014
Objective(s): Regulatory T cells, including CD4+CD25+Fox3+ and CD8+CD28- cells play an important role in regulating the balance between immunity and tolerance.
Ebrahim Kouchaki   +4 more
doaj  

MET variants with activating N‐lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation

open access: yesMolecular Oncology, EarlyView.
MET variants in the N‐lobe of the kinase domain, found in hereditary papillary renal cell carcinoma, require ligand stimulation to promote cell transformation, in contrast to other RTK variants. This suggests that HGF expression in the microenvironment is important for tumor growth in such patients. Their sensitivity to MET inhibitors opens the way for
Célia Guérin   +14 more
wiley   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

open access: yesMolecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita   +1 more
wiley   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

open access: yesMolecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi   +5 more
wiley   +1 more source

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