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首页> 外文期刊>Journal of Cellular Physiology >Ascorbic Acid Induces Necrosis in Human Laryngeal Squamous Cell Carcinoma via ROS, PKC, and Calcium Signaling
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Ascorbic Acid Induces Necrosis in Human Laryngeal Squamous Cell Carcinoma via ROS, PKC, and Calcium Signaling

机译：抗坏血酸诱发人类喉部坏死鳞状细胞癌通过ROS、PKC和钙信号

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Ascorbic acid induces apoptosis, autophagy, and necrotic cell death in cancer cells. We investigated the mechanisms by which ascorbic acid induces death in laryngeal squamous cell carcinoma Hep2 cells. Ascorbic acid markedly reduced cell viability and induced death without caspase activation and an increase in cytochrome c. Hep2 cells exposed to ascorbic acid exhibited membrane rupture and swelling, the morphological characteristics of necrotic cell death. The generation of reactive oxygen species (ROS) was increased in Hep2 cells treated with ascorbic acid, and pretreatment with N-acetylcysteine blocked ascorbic acid-induced cell death. Ascorbic acid also stimulated protein kinase C (PKC) signaling, especially PKC / activation, and subsequently increased cytosolic calcium levels. However, ascorbic acid-induced necrotic cell death was inhibited by Ro-31-8425 (PKC inhibitor) and BAPTA-AM (cytosolic calcium-selective chelator). ROS scavenger NAC inhibited PKC activation induced by ascorbic acid and Ro-31-8425 suppressed the level of cytosolic calcium increased by ascorbic acid, indicating that ROS is represented as an upstream signal of PKC pathway and PKC activation leads to the release of calcium into the cytosol, which ultimately regulates the induction of necrosis in ascorbic acid-treated Hep2 cells. These data demonstrate that ascorbic acid induces necrotic cell death through ROS generation, PKC activation, and cytosolic calcium signaling in Hep2 cells. J. Cell. Physiol. 232: 417-425, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：抗坏血酸诱导细胞凋亡、自噬和在癌症细胞坏死的细胞死亡。调查的机制抗坏血酸诱发喉鳞状细胞死亡癌Hep2细胞。减少细胞的生存能力和诱导死亡半胱天冬酶活化和细胞色素的增加c。Hep2细胞暴露于抗坏血酸展出膜破裂和肿胀,形态坏死细胞死亡的特征。代的活性氧(ROS)增加Hep2细胞治疗抗坏血酸,和预处理防治作用阻止抗坏血段细胞死亡。抗坏血酸也刺激蛋白激酶C(PKC)信号,尤其是PKC激活、和随后胞质钙含量增加。然而,抗坏血段坏死细胞死亡是被ro - 31 - 8425 (PKC抑制剂)和BAPTA-AM(胞质calcium-selective螯合剂)。抗坏血酸和激活ro - 31 - 8425抑制胞质水平增加了抗坏血酸钙,指示ROS是表示为一个上游的信号PKC途径和PKC激活导致的释放到胞质钙,最终调节坏死的感应抗坏血酸洗Hep2细胞。表明抗坏血酸诱导坏死细胞死亡通过活性氧生成,PKC激活和胞质钙信号Hep2细胞。(c) 2016年威利期刊公司。

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