2020
DOI: 10.1016/j.cellsig.2020.109733
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Capsaicin induces mitochondrial dysfunction and apoptosis in anaplastic thyroid carcinoma cells via TRPV1-mediated mitochondrial calcium overload

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Cited by 43 publications
(39 citation statements)
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“…In breast cancer cells lines, apoptosis was induced through cytosolic calcium overload, and was verified by the overexpression of Bax [ 24 ]. Similarly, in thyroid carcinoma cells, interference in mitochondrial calcium regulation triggered caspase stimulation and resulted in apoptosis [ 25 ]. Additionally, calcium signaling can influence ROS generation or MMP, which are other causes of apoptosis.…”
Section: Discussionmentioning
confidence: 99%
“…In breast cancer cells lines, apoptosis was induced through cytosolic calcium overload, and was verified by the overexpression of Bax [ 24 ]. Similarly, in thyroid carcinoma cells, interference in mitochondrial calcium regulation triggered caspase stimulation and resulted in apoptosis [ 25 ]. Additionally, calcium signaling can influence ROS generation or MMP, which are other causes of apoptosis.…”
Section: Discussionmentioning
confidence: 99%
“…TRPC3 is specifically inhibited by Pyr3 (Ethyl-1-(4-(2,3,3-trichloroacrylamide)phenyl)-5-(trifluoromethyl)-1H-pyrazole-4-carboxylate), which has been shown to depolarize the MIM and boost ROS production when applied together with dexamethasone [ 73 ]. In the case of TRPV1, a recent study linked apoptosis induction by capsaicin to mitochondrial calcium overload, although whether mitochondrial TRPV1 is responsible for the effect of this channel agonist has not been specifically addressed [ 74 ]. As to MCUC, a small heterocyclic compound, AG311, (5-[(4-methylphenyl)thio]-9H-pyrimido[4,5- b ]indole-2,4-diamine) was shown to depolarize mitochondria and proposed to exert its tumor growth-retarding effect by activating MCUC [ 75 ].…”
Section: Mitochondrial Ion Channels and Their Pharmacological Targeting By Small Moleculesmentioning
confidence: 99%
“…Among them, oxidative stress signaling has often being highlighted. Given that ROS are generated mainly through the electron transport chain in mitochondria, many reports have emphasized the correlation between mitochondrial disruption and capsaicin-induced apoptosis in cancer cells [46][47][48][49]. Compared to the ROS-dependent apoptotic activity of capsaicin, however, the ability of capsaicin to induce autophagy is relatively less common in the literature.…”
Section: Discussionmentioning
confidence: 99%