Results 61 to 70 of about 279,199 (293)
TRPM8 levels determine tumor vulnerability to channel agonists
Molecular Oncology, EarlyView.TRPM8 is a Ca2+ permissive channel. Regardless of the amount of its transcript, high levels of TRPM8 protein mark different tumors, including prostate, breast, colorectal, and lung carcinomas. Targeting TRPM8 with channel agonists stimulates inward calcium currents followed by emptying of cytosolic Ca2+ stores in cancer cells.
Alessandro Alaimo +18 more
wiley +1 more source
Majallah-i Dānishgāh-i ̒Ulūm-i Pizishkī-i Bābul, 2019 BACKGROUND AND OBJECTIVE: Studies have shown that ibuprofen can have an anti-cancer effect on cervical cells, although the mechanism of this effect is not well known in cellular and molecular terms.
E Ghadiri, R Ahmadi, E Rostami
doaj
Molecular 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
Systematic profiling of cancer‐fibroblast interactions reveals drug combinations in ovarian cancer
Molecular Oncology, EarlyView.Fibroblasts, cells in the tumor environment, support ovarian cancer cell growth and alter morphology and drug response. We used fibroblast and cancer cell co‐culture models to test 528 drugs and discovered new drugs for combination treatment. We showed that adding Vorinostat or Birinapant to standard chemotherapy may improve drug response, suggesting ...
Greta Gudoityte +10 more
wiley +1 more source
BMC Cancer, 2019 Background In epithelial cells, tyrosine kinases induce tyrosine phosphorylation and ubiquitination of the E-cadherin complex, which is responsible for the epithelial-mesenchymal transition (EMT). However, the precise mechanisms remain unclear.
Yunfeng Zhang +5 more
doaj +1 more source
Cell Death and Disease, 2021 The cysteine protease, caspase-8, undergoes dimerization, processing, and activation following stimulation of cells with death ligands such as TRAIL, and mediates TRAIL induction of the extrinsic apoptosis pathway.
Zhibin Cui +5 more
doaj +1 more source
A tumour suppressor function of caspase-8? [PDF]
Cell Death & Differentiation, 2008 Every so often, research throws up something unexpected. Science being inherently conservative, these reports are usually treated with greater rigour at peer review, and journals are often reluctant to publish contentious papers that do not broadly conform to the established dogma, unless the data are wholly compelling and there is a detailed molecular
Richard A. Knight, David L. Vaux
openaire +2 more sources
Genomics‐led approach to drug testing in models of undifferentiated pleomorphic sarcoma
Molecular Oncology, EarlyView.GA text Genomic data from undifferentiated pleomorphic sarcoma patients and preclinical models were used to inform a targeted drug screen. Selected compounds were tested in 2D and 3D cultures of UPS cell lines. A combination of trametinib and infigratinib was synergistic in the majority of UPS cell lines tested, which was further confirmed in an ex ...
Piotr J. Manasterski +19 more
wiley +1 more source
Activation of Caspase-8 in the Alzheimer's Disease Brain
Neurobiology of Disease, 2001 Recent studies support the activation of apoptotic pathways in the Alzheimer's disease (AD) brain. Neurons committed to apoptosis may do so by either activation of a receptor-mediated pathway employing caspase-8 or through an alternative mitochondrial pathway involving oxidative stress.
Rohn, Troy T. +4 more
openaire +5 more sources
Differential Inactivation of Caspase-8 in Lung Cancers [PDF]
Cancer Biology & Therapy, 2002 Caspase-8 (CASP8) is an apoptosis inducing cysteine protease which is activated through the formation of a death-inducing signaling complex when death receptors are complexed to their specific ligands. Recent reports indicate that CASP8 expression is lost via a combination of promoter methylation and allelic loss in subset of neuroblastomas.
Takashi Takahashi +11 more
openaire +3 more sources