Synergetic and Antagonistic Molecular Effects Mediated by the Feedback Loop of p53 and JNK between Saikosaponin D and SP600125 on Lung Cancer A549 Cells

Chen, Xiaoman; Liu, Cheng‐Lin; Zhao, Ruilin; Zhao, Ping; Wu, Ju; Zhou, Nan; Ying, Muying

doi:10.1021/acs.molpharmaceut.8b00595

Cited by 24 publications

(18 citation statements)

References 33 publications

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“…To validate the oxidative stress‐induced increase in miR‐34c is mediated by ROS‐JNK‐P53 pathway, we found that H 2 O 2 induced an increase in intracellular ROS production in HT‐22 cells by flow cytometry (FCM) assay (Figure a) and the JNK activation and P53 accumulation were induced by exogenous H 2 O 2 in a concentration‐dependent manner (Figure b). JNK has been reported to be implicated in P53 accumulation (Chen et al, ; Wu et al, ). Thus, the effect of JNK on P53 accumulation was determined by using of JNK inhibitor SP600125.…”

Section: Resultsmentioning

confidence: 99%

Increased miR‐34c mediates synaptic deficits by targeting synaptotagmin 1 through ROS‐JNK‐p53 pathway in Alzheimer’s Disease

Shi

Zhang

Zhou³

et al. 2020

Aging Cell

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Alzheimer's disease (AD) and cancer have inverse relationship in many aspects. Some tumor suppressors, including miR‐34c, are decreased in cancer but increased in AD. The upstream regulatory pathways and the downstream mechanisms of miR‐34c in AD remain to be investigated. The expression of miR‐34c was detected by RT–qPCR in oxidative stressed neurons, hippocampus of SAMP8 mice, or serum of patients with amnestic mild cognitive impairment (aMCI). Dual luciferase assay was performed to confirm the binding sites of miR‐34c in its target mRNA. The Morris water maze (MWM) was used to evaluate learning and memory in SAMP8 mice administrated with miR‐34c antagomir (AM34c). Golgi staining was used to evaluate the synaptic function and structure. The dramatically increased miR‐34c was mediated by ROS‐JNK‐p53 pathway and negatively regulated synaptotagmin 1 (SYT1) expression by targeting the 3′‐untranslated region (3′‐UTR) of syt1 in AD. The expression of SYT1 protein was reduced by over expression of miR‐34c in the HT‐22 cells and vice versa. Administration of AM34c by the third ventricle injection or intranasal delivery markedly increased the brain levels of SYT1 and ameliorated the cognitive function in SAMP8 mice. The serum miR‐34c was significantly increased in patients with aMCI and might be a predictive biomarker for diagnosis of aMCI. These results indicated that increased miR‐34c mediated synaptic and memory deficits by targeting SYT1 through ROS‐JNK‐p53 pathway and the miR‐34c/SYT1 pathway could be considered as a promising novel therapeutic target for patients with AD.

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Section: Resultsmentioning

confidence: 99%

Increased miR‐34c mediates synaptic deficits by targeting synaptotagmin 1 through ROS‐JNK‐p53 pathway in Alzheimer’s Disease

Shi

Zhang

Zhou³

et al. 2020

Aging Cell

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“…A review of the literature reveals the relevant situation downstream of JNK. For example, IL-2/sorafenib can affect tumor survival, growth and mobility through JNK-TAZ pathways (41), GPS1 can activate the c-Jun N-terminal kinase (JNK)/Jun pathway to affect breast cancer growth and migration (42), Saikosaponin D induced apoptosis via the activation of TGFα-JNK-p53 (43), Thymoquinone inhibits the metastasis through activation of JNK-p38 (44), JNK-ELK1 The pathway can also have an effect on the tumor (45). These are the pathways already known downstream of JNK, but there must be downstream pathways that have not been studied.…”

Section: Discussionmentioning

confidence: 99%

NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT

Meng

Wu²,

Huang

et al. 2019

Oncol Lett

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Neural precursor cell-expressed, developmentally-downregulated 9 (NEDD9) is a multi-domain skeleton protein that serves an important role in the cell signaling process via modulating invasion, metastasis, proliferation and apoptosis of tumor cells. The present study identified that the expression levels of NEDD9 in colorectal cancer were elevated. Therefore, the effect of downregulating the expression of NEDD9 in terms of invasion and migration of colorectal cancer cells was investigated and the role of the JNK pathway in these processes was also investigated. The data revealed that downregulation of NEDD9 and JNK inhibitors suppressed invasion and migration, decreased expression levels of phosphorylated JNK, increased the expression levels of E-cadherin and decreased the expression levels of vimentin. In summary, NEDD9 promotes invasion and migration of colorectal cancer cells via the JNK pathway.

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“…[15] Drugs related to cell cycle regulators act on the synergetic and antagonistic feedback loop formed by JNK / pJNK and p53 / p53. [16] Via WSSV-IE1, white spot syndrome virus (WSSV) combines with JNK and enhances JNK activation through self-phosphorylation, then establishes a positive feedback loop of JNK mediated by virus gene. [17] 3 JNK AND DEPRESSION…”

Section: Factors Affecting Jnkmentioning

confidence: 99%

Relationship Between c-Jun N-terminal Kinase and Depression

2020

E3S Web Conf.

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Depression is one of the most common emotional disorders. The cause of depression is still not clear. C-Jun N-terminal kinase (JNK) is one number of mitogen activated protein kinase (MAPK) family, which is closely related to the occurrence of many diseases. At present, it is believed that JNK plays an important role in the parthenogenesis of depression, but the specific mechanism is not clear. This review will focus on the possible mechanism of JNK protein and JNK signaling pathway affecting the parthenogenesis of depression.

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Synergetic and Antagonistic Molecular Effects Mediated by the Feedback Loop of p53 and JNK between Saikosaponin D and SP600125 on Lung Cancer A549 Cells

Cited by 24 publications

References 33 publications

Increased miR‐34c mediates synaptic deficits by targeting synaptotagmin 1 through ROS‐JNK‐p53 pathway in Alzheimer’s Disease

Increased miR‐34c mediates synaptic deficits by targeting synaptotagmin 1 through ROS‐JNK‐p53 pathway in Alzheimer’s Disease

NEDD9 promotes invasion and migration of colorectal cancer cell line HCT116 via JNK/EMT

Relationship Between c-Jun N-terminal Kinase and Depression

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