l -抗坏血酸通过调节活化B细胞/丝裂原活化蛋白激酶/Akt信号通路的核因子kappa-轻链增强子诱导人喉表皮样Hep-2细胞凋亡

J. Park, Yoon-Jung Kim, S. Park, Kyung-Yi Chung, Sang-Jin Oh, Won-Jae Kim, Ji-Yeon Jung
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引用次数: 0

摘要

l -抗坏血酸(L-AA;维生素C)诱导癌细胞凋亡。本研究旨在阐明l - aa诱导人喉部表皮样癌Hep-2细胞凋亡的分子机制。L-AA抑制Hep-2细胞活力,诱导凋亡,表现为核染色质的切割和凝聚,Annexin v阳性细胞数量增加。L-AA降低Bcl-2蛋白表达,上调Bax蛋白水平。此外,L-AA处理增强了细胞色素c从线粒体释放到胞质中,并促进了caspase-9、-8和-3的活化。此外,凋亡诱导因子(AIF)和内切酶G (EndoG)在l - aa处理的Hep-2细胞凋亡过程中易位到细胞核内。L-AA可有效抑制构成性核因子-κB (NF-κB)的活化,减弱NF-κB p65亚基的核表达。有趣的是,L-AA处理Hep-2细胞可显著激活Akt和丝裂原活化蛋白激酶(MAPK;细胞外信号调节激酶1/2、p38和c-Jun n -末端激酶[JNK])和LY294002 (Akt抑制剂)、SB203580 (p38抑制剂)或SP600125 (JNK抑制剂)降低Annexin v阳性细胞的水平。这些结果表明,L-AA通过调节Bcl- 2家族和MAPK/Akt信号通路,通过AIF和EndoG的核易位诱导Hep-2细胞凋亡。
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L-ascorbic acid induces apoptosis in human laryngeal epidermoid Hep-2 cells by modulating the nuclear factor kappa-light-chain-enhancer of activated B cells/ mitogen-activated protein kinase/Akt signaling pathway
L-ascorbic acid (L-AA; vitamin C) induces apoptosis in cancer cells. This study aimed to elucidate the molecular mechanisms of L-AA-induced apoptosis in human laryngeal epidermoid carcinoma Hep-2 cells. L-AA suppressed the viability of Hep-2 cells and induced apoptosis, as shown by the cleavage and condensation of nuclear chromatin and increased number of Annexin V-positive cells. L-AA decreased Bcl-2 protein expression but upregulated Bax protein levels. In addition, cytochrome c release from the mitochondria into the cytosol and activation of caspase-9, -8, and -3 were enhanced by L-AA treatment. Furthermore, apoptosis-inducing factor (AIF) and endonuclease G (EndoG) were translocated into the nucleus during apoptosis of L-AA-treated Hep-2 cells. L-AA effectively inhibited the constitutive nuclear factor-κB (NF-κB) activation and attenuated the nuclear expression of the p65 subunit of NF-κB. Interestingly, L-AA treatment of Hep-2 cells markedly activated Akt and mitogen-activated protein kinase (MAPK; extracellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase [JNK]) and and LY294002 (Akt inhibitor), SB203580 (p38 inhibitor) or SP600125 (a JNK inhibitor) decreased the levels of Annexin V-positive cells. These results suggested that L-AA induces the apoptosis of Hep-2 cells via the nuclear translocation of AIF and EndoG by modulating the Bcl- 2 family and MAPK/Akt signaling pathways.
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