2018
DOI: 10.1016/j.bbrc.2017.11.199
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Chetomin induces apoptosis in human triple-negative breast cancer cells by promoting calcium overload and mitochondrial dysfunction

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Cited by 28 publications
(18 citation statements)
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“…For chaetomin, its sperm motility-inhibiting effect may be explained in terms of mitochondrial toxicity. Chaetomin is known to induce cell apoptosis by disrupting the mitochondrial function and by promoting calcium overload [46]. For chaetoglobosin, its sperm motility-inhibiting effect and cytostatic effect could be very likely explained by its glucose transport-inhibiting activity [23,33].…”
Section: Discussionmentioning
confidence: 99%
“…For chaetomin, its sperm motility-inhibiting effect may be explained in terms of mitochondrial toxicity. Chaetomin is known to induce cell apoptosis by disrupting the mitochondrial function and by promoting calcium overload [46]. For chaetoglobosin, its sperm motility-inhibiting effect and cytostatic effect could be very likely explained by its glucose transport-inhibiting activity [23,33].…”
Section: Discussionmentioning
confidence: 99%
“…Due to the inhibition of HIF-1α, chetomin was ( 52 ) reported to decrease invasiveness in MDA-MB-231 triple negative breast cancer cells under hypoxic conditions [167]. More recently, 52 was also found to induce apoptosis in human triple-negative breast cancer cells by mitochondrial dysfunction, through the inhibition of PI3K/mTOR induced ER stress and promotion of calcium overload [168]. In fact, additional molecular mechanisms underlying chetomin ( 52 ) anticancer effects have been reported.…”
Section: Chemistry and Biological Properties Of Marine Diketopipermentioning
confidence: 99%
“…24 Dewangan J et al have demonstrated that in triple-negative breast cancer, calcium overload in mitochondria can lead to the release of cytochrome c, which in turn triggers caspase-3 mediated cell death, while inhibition of calcium signaling using BAPTA-AM can reduce apoptosis, thus confirming that calcium signaling is involved in chetomin-induced cell death. 25 Other experts have confirmed that Fe(III) in cells can be further reduced to ferrous ions, which interacts with dihydroartemisinin to increase the toxicity of tumor cells. The increased accumulation of dihydroartemisinin in tumor cells, and the joint release activation mechanism of dihydroartemisinin and Fe(III), especially under the guidance of an externally applied magnetic field, have demonstrated the potential of this antitumor in vivo.…”
Section: Discussionmentioning
confidence: 99%