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Aplidin™ induces the mitochondrial apoptotic pathway via oxidative stress-mediated JNK and p38 activation and protein kinase C δ
TLDR
It is demonstrated that protein kinase C delta (PKC-δ) mediates the cytotoxic effect of Aplidin™ and that it is concomitantly processed and activated late in the apoptotic process by a caspase mediated mechanism. Expand
Plitidepsin has potent preclinical efficacy against SARS-CoV-2 by targeting the host protein eEF1A
TLDR
The results indicate that plitidepsin is a promising therapeutic candidate for COVID-19, and in cells, the drug is substantially more potent than remdesivir against SARS-CoV-2, with limited cellular toxicity. Expand
AplidinTM Induces Apoptosis in Human Cancer Cells via Glutathione Depletion and Sustained Activation of the Epidermal Growth Factor Receptor, Src, JNK, and p38 MAPK*
TLDR
AplidinTM induced growth arrest and apoptosis in human MDA-MB-231 breast cancer cells at nanomolar concentrations and induced apoptosis and activated EGFR, JNK, and p38 MAPK in two cell lines derived from human renal cancer, a neoplasia that is highly refractory to chemotherapy. Expand
Translation Elongation Factor eEF1A2 is a Novel Anticancer Target for the Marine Natural Product Plitidepsin
TLDR
It is demonstrated that plitidepsin exerts its antitumor activity by targeting eEF1A2, one of the isoforms of the alpha subunit of the eukaryotic Elongation Factor 1, which is endowed with oncogenic properties, favoring tumor cell proliferation while inhibiting apoptosis. Expand
Antitumor actinopyranones produced by Streptomyces albus POR-04-15-053 isolated from a marine sediment.
TLDR
Members of the pyranone family of compounds could be developed as potential antitumor agents, according to their structures and cytotoxicity results. Expand
The mechanism of action of plitidepsin.
TLDR
This review outlines the current knowledge of plitidepsin activity, with a primary focus on the molecular mechanisms of action of the compound. Expand
Generation of endoplasmic reticulum stress and inhibition of autophagy by plitidepsin induces proteotoxic apoptosis in cancer cells.
TLDR
It is revealed that PLD induces an increase in the levels of misfolded proteins while simultaneously inhibiting the autophagic flux, which combined prevent PLD-treated cells from reducing proteotoxic stress and lead to apoptosis. Expand
Binding of eEF1A2 to the RNA-dependent protein kinase PKR modulates its activity and promotes tumour cell survival
TLDR
It is uncovered that double-stranded RNA-activated protein kinase (PKR) is a novel eEF1A2-interacting partner whose pro-apoptotic effect is hindered by the translation factor, most likely through sequestration and inhibition of its kinase activity. Expand
Establishment and characterisation of a human carcinoma cell line with acquired resistance to Aplidin™
TLDR
It is suggested that sustained activation of JNK and p38 is essential for triggering the apoptotic programme induced by APL and that HeLa-APL cells bypass this apoptotic response by preventing the specific mechanisms that prime and sustain the long-term activation of these signalling cascades. Expand
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