Cross‐talk of alpha tocopherol‐associated protein and JNK controls the oxidative stress‐induced apoptosis in prostate cancer cells

Zhu, Baoyi; Li, Xiaojuan; Ye, Chunwei; Wang, Yu; Cai, Sanjun; Huang, Huaiqiu; Cai, Yi; Yeh, Shuyuan; Huang, Zhenhua; Chen, Ruihan; Tao, Yiran; Wen, Xin

doi:10.1002/ijc.27927

Cited by 15 publications

(10 citation statements)

References 39 publications

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“…Activated JNK can transmit extracellular signals to regulate cell proliferation, apoptosis and autophagy in response to chemotherapeutic agents1314. The JNK signaling pathway has been shown to be closely associated with the resistance to several antitumor agents such as cisplatin, mitoxantrone, docetaxel and oxaliplatin15161718. However, no relationship has been reported between 5-FU resistance caused by mutations or deletions of p53 and the JNK signaling pathway.…”

mentioning

confidence: 99%

RETRACTED ARTICLE: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy

Sui

Kong

Wang

et al. 2014

Sci Rep

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Deficiency or mutation in the p53 tumor suppressor gene commonly occurs in human cancer and can contribute to disease progression and chemotherapy resistance. Currently, although the pro-survival or pro-death effect of autophagy remains a controversial issue, increasing data seem to support the idea that autophagy facilitates cancer cell resistance to chemotherapy treatment. Here we report that 5-FU treatment causes aberrant autophagosome accumulation in HCT116 p53−/− and HT-29 cancer cells. Specific inhibition of autophagy by 3-MA, CQ or small interfering RNA treatment targeting Atg5 or Beclin 1 can potentiate the re-sensitization of these resistant cancer cells to 5-FU. In further analysis, we show that JNK activation and phosphorylation of Bcl-2 are key determinants in 5-FU-induced autophagy. Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53−/− and HT29 cells. Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53−/− and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation. These results provide a promising strategy to improve the efficacy of 5-FU-based chemotherapy for colorectal cancer patients harboring a p53 gene mutation.

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mentioning

confidence: 99%

RETRACTED ARTICLE: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy

Sui

Kong

Wang

et al. 2014

Sci Rep

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“…Together, these data indicate that HVJ‐E activates the three main MAPK pathways in B16F10 cells upstream of caspase activation. However, in the current experiment, among the three main MAPK pathways, Jnk was robustly activated, which is often linked with mitochondrial damage, ROS production and the subsequent initiation of the mitochondrial death pathway . In addition, the release of Cytochrome C in cells post HVJ‐E treatment was also observed.…”

Section: Resultsmentioning

confidence: 54%

“…However, in the current experiment, among the three main MAPK pathways, Jnk was robustly activated, which is often linked with mitochondrial damage, ROS production and the subsequent initiation of the mitochondrial death pathway. 27,28 In addition, the release of Cytochrome C in cells post HVJ-E treatment was also observed. So, the ROS generation and mitochondrial membrane potential in HVJ-E-treated cells were detected.…”

Section: Mapk Signaling Pathways Play a Role In Hvj-e-induced Apoptosmentioning

confidence: 93%

IPS‐1 plays a dual function to directly induce apoptosis in murine melanoma cells by inactivated Sendai virus

Zhang

Yuan

et al. 2013

Intl Journal of Cancer

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Inactivated Sendai virus (HVJ-E) directly kills cancer cells by inducing apoptosis through a mechanism mediated by Janus kinases=signal transducers and activators of transcription (JAK=STAT) signaling pathways. However, whether other signaling pathways are involved remain largely unknown. This study aimed to investigate the mechanism underlying HVJ-E-induced apoptosis in murine B16F10 melanoma cells. We found that HVJ-E induced B16F10 cell apoptosis via the caspase pathway, particularly caspase-9, which mediates the intrinsic apoptotic pathway. Mitogen-activated protein kinase (MAPK) pathway activation also contributed to HVJ-E-induced apoptosis. Whereas caspase pathway involvement depended on both IFN-b promoter stimulator-1 (IPS-1) and type I interferon (IFN), MAPK pathway activation was independent of type I IFN but involved IPS-1. In addition, intratumoral HVJ-E treatment displayed a direct oncolytic effect in an in vivo BALB=c nude mouse melanoma model. Collectively, our data provides new insights into the mechanism underlying HVJ-E-induced apoptosis in tumor cells.

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“…AP-1 is involved in many different important cellular processes, including proliferation, differentiation, and apoptosis [47]. First, we analyzed the effect of 15 μmol/l RG003 on the activation of NF-κB and AP-1.…”

Section: Rg003 Induces Downregulation Of Survival Pathways In Pc-3 Cellsmentioning

confidence: 99%

2′-Hydroxy-4-methylsulfonylchalcone enhances TRAIL-induced apoptosis in prostate cancer cells

Ismail¹,

Fagnere²,

Limami³

et al. 2015

Anti-Cancer Drugs

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Prostate cancer is the most common malignant cancer in men and the second leading cause of cancer deaths. Previously, we have shown that 2'-hydroxy-4-methylsulfonylchalcone (RG003) induced apoptosis in prostate cancer cell lines PC-3 and DU145. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent, some cancer cells are resistant to TRAIL treatment. PC-3 and LNCaP prostatic cancer cell lines have been reported to be resistant to TRAIL-induced apoptosis. Here, we show for the first time that RG003 overcomes TRAIL resistance in prostate cancer cells. RG003 can enhance TRAIL-induced apoptosis through DR5 upregulation and downregulation of Bcl-2, PI3K/Akt, NF-κB, and cyclooxygenase-2 (COX-2) survival pathways. When used in combined treatment, RG003 and TRAIL amplified TRAIL-induced activation of apoptosis effectors and particularly activation of caspase-8 and the executioner caspase-3, leading to increased poly-ADP-ribose polymerase cleavage and DNA fragmentation in prostate cancer cells. Furthermore, we showed that RG003 reduced COX-2 expression in cells. Previously, we showed that COX-2 was involved in resistance to an apoptosis mechanism; then, its inhibition by RG003 could render cells more sensitive to TRAIL treatment. We showed that nuclear factor-κB activation was inhibited after RG003 treatment. This inhibition was correlated with reduction in COX-2 expression and induction of apoptosis. Overall, we conclude, for the first time, that RG003 can enhance TRAIL-induced apoptosis in human prostate cancer cells. The significance of our in-vitro study with RG003 and TRAIL combined is very encouraging, suggesting the relevance of testing this combined treatment in xenograft animal models.

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Cross‐talk of alpha tocopherol‐associated protein and JNK controls the oxidative stress‐induced apoptosis in prostate cancer cells

Cited by 15 publications

References 39 publications

RETRACTED ARTICLE: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy

RETRACTED ARTICLE: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy

IPS‐1 plays a dual function to directly induce apoptosis in murine melanoma cells by inactivated Sendai virus

2′-Hydroxy-4-methylsulfonylchalcone enhances TRAIL-induced apoptosis in prostate cancer cells

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