Inhibition of JNK3 Promotes Apoptosis Induced by BH3 Mimetic S1 in Chemoresistant Human Ovarian Cancer Cells

Yang, Xiaochun; Xiang, Xiyan; Xia, Meihui; Su, Jing; Wu, Yao; Shen, Luyan; Xu, Ye; Sun, Liankun

doi:10.1002/ar.22991

Cited by 22 publications

(17 citation statements)

References 41 publications

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“…In our study, we revealed that H19 was aberrantly upregulated in breast tumor tissues and breast cancer cells MCF‐7 and MDA‐MB‐231. In accordance with the previous studies, H19 downregulation was found to inhibit cell proliferation and invasion of breast cancer cells, indicating that H19 acted as an oncogene and upregulation of H19 played a crucial role in breast cancer. Consistently, H19 was highly expressed and played oncogenic role by promoting cell proliferation in cervical cancer and pancreatic ductal adenocarcinoma .…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152

et al. 2017

J Biochem Mol Toxicol

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Long non-coding RNA (lncRNA) H19 in tumors played important roles in various biological processes. However, the biological role and molecular mechanism of H19 in breast cancer are unclear. Here, we found that H19 was aberrantly upregulated in human breast tumor tissues and cells. A negative correlation between H19 and miR-152 and positive correlation between H19 and DNMT1 mRNA were observed. Downregulation of H19 and DNMT1 significantly retarded breast cancer cell proliferation and invasion. H19 act as an endogenous sponge by directly binding to miR-152. miR-152 directly targeted DNMT1 and was regulated by H19. Besides, H19 overexpression dramatically relieved the inhibition of miR-152 on DNMT1 expression. miR-152 inhibition and DNMT1 overexpression obviously reversed the inhibitory effects of H19 downregulation on cell proliferation and invasion. In conclusion, H19 promoted proliferation and invasion of breast cancer through the miR-152/DNMT1 axis, providing a novel mechanism about the occurrence and development of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152

et al. 2017

J Biochem Mol Toxicol

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“…However, the exact molecular mechanism of this phenomenon and whether there is crosstalk with other WNT signalling pathways are unclear. A previous study showed that inhibition of JNK3 upregulates the production of reactive oxygen species (ROS) and thereby increases the rate of apoptosis (Yang et al, ), while another study showed that EGCG induces apoptosis of primary endothelial cells by decreasing JNK‐mediated catalase activity (Kim et al, ). Thus, the effect of EGCG may be mediated by an increase in ROS, and EGCG‐induced ROS and oxidative stress, as well as their relationship with the WNT/JNK pathway, warrant future research.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin‐3‐gallate inhibits proliferation and induces apoptosis in odontogenic keratocyst keratinocytes

et al. 2019

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Objective The aim of this study was to investigate the effects of epigallocatechin‐3‐gallate on the proliferation and apoptosis of odontogenic keratocyst (OKC) keratinocytes in vitro. Materials and methods Keratinocytes isolated from the epithelial lining of the OKC were cultured in keratinocyte serum‐free medium and identified by CK10, CK14, pan‐cytokeratin and vimentin immunofluorescence staining. The cells were exposed to EGCG at different concentrations, and proliferation inhibition was measured by cell counting kit 8 assay. Cell cycle and apoptosis were assessed by flow cytometry, and expression of the WNT signalling pathway‐related proteins FZD3 and JNK3 was detected by quantitative real‐time PCR and Western blotting. Human oral keratinocytes (HOKs) were used as the control. Results The OKC keratinocytes were successfully cultured. The primary cells were tile‐like and expressed the epithelial biomarkers CK10, CK14 and pan‐cytokeratin. Epigallocatechin‐3‐gallate inhibited cell proliferation in a dose‐ and time‐dependent manner, arrested cell cycle in the G1 phase and induced apoptosis of OKC keratinocytes. FZD3 and JNK3 were overexpressed in OKC keratinocytes compared with HOKs and were downregulated by epigallocatechin‐3‐gallate treatment. Conclusion Epigallocatechin‐3‐gallate inhibited proliferation and induced apoptosis in OKC keratinocytes, possibly by suppressing the WNT/JNK signalling pathway. It may thus be potentially used for OKC treatment.

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“…4B). Since p62 is one of the substrate proteins degraded through autophagy, its expression is an indicator of autophagy flux (27,28). These data implied that autophagy flux changed with increased ER stress.…”

Section: Differential Activation Of the Map-kinase P38 Jnk And Erk Imentioning

confidence: 94%

Inhibition of autophagic flux by ROS promotes apoptosis during DTT-induced ER/oxidative stress in HeLa cells

Xiang

Yang

et al. 2016

Oncology Reports

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Abstract. As targets for cancer therapy, endoplasmic reticulum (ER) stress and autophagy are closely linked. However, the signaling pathways responsible for induction of autophagy in response to ER stress and its cellular consequences appear to vary with cell type and stimulus. In the present study, we showed that dithiothreitol (DTT) induced ER stress in HeLa cells in a time-and dose-dependent fashion. With increased ER stress, reactive oxygen species (ROS) production increased and autophagy flux, assessed by intracellular accumulation of LC3B-II and p62, was inhibited. N-acetyl-L-cysteine (NAC), a classic antioxidant, exacerbated cell death induced by 3.2 mM of DTT, but attenuated that induced by 6.4 mM DTT. Low cytotoxic doses of DTT transiently activated c-JNU N-terminal kinase (JNK) and p38, whereas high dose of DTT persistently activated JNK and p38 and simultaneously reduced extracellular signal-regulated kinase (ERK) activity. Combined treatment with DTT and U0126, an inhibitor of ERK upstream activators mitogen-activated protein kinase (MAPK) kinase 1 and 2 (MEK1/2), blocked autophagy flux in HeLa cells. This effect was similar to that caused by a combination of DTT and chloroquine (CQ). These data suggested that insufficient autophagy was accompanied by increased ROS production during DTT-induced ER stress. ROS appeared to regulate MAPK signaling, switching from a pro-survival to a pro-apoptotic signal as ER stress increased. ERK inhibition by ROS during severe ER stress blocked autophagic flux. Impaired autophagic flux, in turn, aggravated ER stress, ultimately leading to cell death. Taken together, our data provide the first reported evidence that ROS may control cell fate through regulating the MAPK pathways and autophagic flux during DTT-induced ER/oxidative stress.

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Inhibition of JNK3 Promotes Apoptosis Induced by BH3 Mimetic S1 in Chemoresistant Human Ovarian Cancer Cells

Cited by 22 publications

References 41 publications

Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152

Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152

Epigallocatechin‐3‐gallate inhibits proliferation and induces apoptosis in odontogenic keratocyst keratinocytes

Inhibition of autophagic flux by ROS promotes apoptosis during DTT-induced ER/oxidative stress in HeLa cells

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