TNFR1/TNF-α and mitochondria interrelated signaling pathway mediates quinocetone-induced apoptosis in HepG2 cells

Zhang, Chaoming; Wang, Congcong; Tang, Shusheng; Sun, Yu; Zhao, Dongxu; Zhang, Shen; Deng, Shumin; Zhou, Yan; Xiao, Xilong

doi:10.1016/j.fct.2013.10.022

Cited by 44 publications

(26 citation statements)

References 41 publications

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“…The balance between the expression levels of Bcl-2 and Bax is important for cell survival and death [27][28][29]. Increased Bax/Bcl-2 ratio usually contributes to relative higher cell apoptosis via caspase activation through mitochondrial pathway [29][30][31][32]. Interestingly, our results showed the knockdown of Anxa11 decreases cell apoptosis with increased Bax/Bcl-2 ratio (Fig.…”

Section: Discussionsupporting

confidence: 45%

Annexin A11 knockdown inhibits in vitro proliferation and enhances survival of Hca-F cell via Akt2/FoxO1 pathway and MMP-9 expression

Liu

Wang

Guo

et al. 2015

Biomedicine & Pharmacotherapy

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Section: Discussionsupporting

confidence: 45%

Annexin A11 knockdown inhibits in vitro proliferation and enhances survival of Hca-F cell via Akt2/FoxO1 pathway and MMP-9 expression

Liu

Wang

Guo

et al. 2015

Biomedicine & Pharmacotherapy

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“…Tissue lysate samples were centrifuged at 145,000 ϫ g for 15 min at 4°C, and protein concentration was measured using the BCA protein assay kit. Western blotting was conducted with 100 g protein per lane (32). The following primary antibodies were employed: rabbit polyclonal antibodies against cleaved caspase-3 (1:1,000), cleaved caspase-9 (1:1,000), Beclin-1 (1:2,000), LC3B (1: 1,000), p53 (1:1,000), p21 (1:1,000), Bcl-2 (1:1,000), caspase-3 (1: 1,000), cyclin-dependent kinase 2 (CDK2) (1:1,000), apoptosis-induced factor (AIF) (1:2,000), cytochrome C (cytC) (1:2,000; Santa Cruz Biotechnology, Inc.), activating transcription factor 6 (ATF6; 1:1,000), growth arrest and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) (1:1,000), glucose-regulated protein 78 kDa/Bax-inhibiting peptide (GRP78/Bip; 1:1,000), Bid (1:1,000), Bax (1:1,000), caspase-9, nuclear factor kappa-light-chain enhancer of activated B cells (NF-B/p65) (1:1,000) (ProteinTech Group, Inc., Chicago, IL, USA), caspase-8 (1:1,000), Fas (1:1,000), p38 (1:1,000); Fas ligand (FasL; 1:1,000), poly(ADP-ribose) polymerase (PARP-1) (1:1,000) (Beyotime Institute of Biotechnology Co., Ltd., Haimen, Jiangsu, China), p-Janus kinase (JNK)/stress-activated protein kinase (SAPK) (1:1,000) (Cell Signaling Technology, Beverly, MA, USA); and mouse monoclonal antibody against p-p38 (1:1,000), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (1:1,000), and ␤-actin (1:1,000; Santa Cruz Biotechnology).…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

Colistin-Induced Nephrotoxicity in Mice Involves the Mitochondrial, Death Receptor, and Endoplasmic Reticulum Pathways

Dai

Tang

et al. 2014

Antimicrob Agents Chemother

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c Nephrotoxicity is the dose-limiting factor for colistin, but the exact mechanism is unknown. This study aimed to investigate the roles of the mitochondrial, death receptor, and endoplasmic reticulum pathways in colistin-induced nephrotoxicity. Mice were intravenously administered 7.5 or 15 mg of colistin/kg of body weight/day (via a 3-min infusion and divided into two doses) for 7 days. Renal function, oxidative stress, and apoptosis were measured. Representative biomarkers involved in the mitochondrial, death receptor, and endoplasmic reticulum pathways were investigated, and the key markers involved in apoptosis and autophagy were examined. After 7-day colistin treatment, significant increase was observed with blood urea nitrogen, serum creatinine, and malondialdehyde, while activities of superoxide dismutase (SOD) and catalase decreased in the kidneys. Acute tubular necrosis and mitochondrial dysfunction were detected, and colistin-induced apoptosis was characterized by DNA fragmentation, cleavage of poly(ADP-ribose) polymerase (PARP-1), increase of 8-hydroxydeoxyguanosine (8-OHdG), and activation of caspases (caspase-8, -9, and -3). It was evident that colistin-induced apoptosis involved the mitochondrial pathway (downregulation of Bcl-2 and upregulation of cytochrome C [cytC] and Bax), death receptor pathway (upregulation of Fas, FasL, and Fasassociated death domain [FADD]), and endoplasmic reticulum pathway (upregulation of Grp78/Bip, ATF6, GADD153/CHOP, and caspase-12). In the 15-mg/kg/day colistin group, expression of the cyclin-dependent kinase 2 (CDK2) and phosphorylated JNK (p-JNK) significantly increased (P < 0.05), while in the 7.5-mg/kg/day colistin group, a large number of autophagolysosomes and classic autophagy were observed. Western blot results of Beclin-1 and LC3B indicated that autophagy may play a protective role in colistin-induced nephrotoxicity. In conclusion, this is the first study to demonstrate that all three major apoptosis pathways and autophagy are involved in colistin-induced nephrotoxicity.

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“…While investigating the underlying proapoptotic mechanisms of ZJW extracts on DDP-induced apoptosis in SGC-7901/DDP cells, we found that the synergistic effect of ZJW extracts on proapoptosis of DDP in SGC-7901/DDP cells might be dependent on the activation of JNK, which played vital role in the development of cancer [20, 21]. Upon activation of JNK, the p-JNK blocked the Bax level and promoted the Bcl-2 level.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effect of Zuo Jin Wan on DDP‐Induced Apoptosis in Human Gastric Cancer SGC‐7901/DDP Cells

Tang

Qiu

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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A traditional Chinese medicine (TCM) formula, Zuo Jin Wan (ZJW), has been found as an anticancer drug in human cancer. In this study, we investigated the synergistic effect of ZJW extracts on DDP-induced apoptosis in human gastric cancer SGC-7901/DDP cells. Our results demonstrated that ZJW extracts could increase the sensitivity of SGC-7901/DDP cells to DDP by increasing the concentration of DDP in cytoplasm and enhance the proapoptosis of DDP by upregulating the JNK and Bax expression, downregulating the Bcl-2 expression, increasing the accumulation of Cytochrome C in cytoplasm, and promoting the activities of caspase-3 and caspase-9. In vivo, ZJW extracts enhanced the inhibiting effect of DDP on tumor growth in SGC-7901/DDP xenograft model and upregulated the expression of p-JNK and Bax but downregulated the Bcl-2 expression in xenograft tumors. In conclusion, in vitro and in vivo, ZJW extracts could enhance the proapoptotic effect of DDP by promoting the activation of JNK and the expression of Bcl-2, inhibiting the Bax expression, followed by increasing the release of Cytochrome C from mitochondria to cytoplasm, and finally activating the caspase cade reaction. Our results implied that ZJW might serve as a synergistic drug with chemotherapeutic drugs DDP in the treatment of gastric cancer.

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TNFR1/TNF-α and mitochondria interrelated signaling pathway mediates quinocetone-induced apoptosis in HepG2 cells

Cited by 44 publications

References 41 publications

Annexin A11 knockdown inhibits in vitro proliferation and enhances survival of Hca-F cell via Akt2/FoxO1 pathway and MMP-9 expression

Annexin A11 knockdown inhibits in vitro proliferation and enhances survival of Hca-F cell via Akt2/FoxO1 pathway and MMP-9 expression

Colistin-Induced Nephrotoxicity in Mice Involves the Mitochondrial, Death Receptor, and Endoplasmic Reticulum Pathways

Synergistic Effect of Zuo Jin Wan on DDP‐Induced Apoptosis in Human Gastric Cancer SGC‐7901/DDP Cells

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