Su, J.; Xu, T.; Jiang, G.; Liang, M.; Cheng, H.; Hou, M.; Li, Q. Gambogenic Acid Triggers Apoptosis of Human Nasopharyngeal Carcinoma CNE-2Z Cells through Activating Volume-Sensitive Outwardly Rectifying Chloride Channels. Preprints2018, 2018060141. https://doi.org/10.20944/preprints201806.0141.v1
APA Style
Su, J., Xu, T., Jiang, G., Liang, M., Cheng, H., Hou, M., & Li, Q. (2018). Gambogenic Acid Triggers Apoptosis of Human Nasopharyngeal Carcinoma CNE-2Z Cells through Activating Volume-Sensitive Outwardly Rectifying Chloride Channels. Preprints. https://doi.org/10.20944/preprints201806.0141.v1
Chicago/Turabian Style
Su, J., Mei Hou and Qinglin Li. 2018 "Gambogenic Acid Triggers Apoptosis of Human Nasopharyngeal Carcinoma CNE-2Z Cells through Activating Volume-Sensitive Outwardly Rectifying Chloride Channels" Preprints. https://doi.org/10.20944/preprints201806.0141.v1
Abstract
Nasopharyngeal carcinoma (NPC) has not been thoroughly studied, and the pathogenesis of NPC is unclear. Scientists have neither discovered effective therapies nor achieved a desirable prognosis. Some studies have found that the regulation of intra- and extracellular ion channels hinges directly on cell apoptosis, and treatment with Gambogenic acid (GNA) brings changes to the volume-sensitive outwardly rectifying chloride (VSOR Cl-) current of CNE-2Z cells recorded by the patch clamp method. Nevertheless, rarely have any researchers probed into the relevance between this variation and the anti-tumor mechanism of GNA. This paper is suggested that GNA activates the VSOR Cl- current on the CNE-2Z cell membrane, and the activation of VSOR Cl- currents by GNA in CNE-2Z cells is blocked by the chloride channel blockers DIDS and DCPIB. GNA induces the down-regulation of GRP78 and up-regulation of ATF4 as well as chop proteins, which is evidence for the induction of CNE-2Z cell apoptosis, and this correlates with ER stress. GNA can activate the VSOR Cl- channel and lead to the occurrence of ER stress, thus inducing the apoptosis of CNE-2Z cells and inhibiting the proliferation of CNE-2Z cells.
Medicine and Pharmacology, Pharmacology and Toxicology
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