ArticleOpen life sciences2019
Nurr1 Promotes Lung Cancer Apoptosis Via Enhancing Mitochondrial Stress and p53-Drp1 Pathway.
Article in Open life sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- miR-125b Attenuates Sepsis-Induced Hippocampal Mitochondrial Fission and Cognitive Impairment via the ROS/p53 Pathway.Molecular neurobiology · 2026Article
- New genetic insights into immunotherapy outcomes in gastric cancer via single-cell RNA sequencing and random forest model.Cancer immunology, immunotherapy : CII · 2024Article
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Authors and funding
7 authors.
Funding
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Abstract
objectiveMitochondrial homeostasis is vital for the progression of lung cancer. Nurr1 has been identified as a novel mediator of mitochondrial homeostasis in several types of cancers. The aim of our study was to investigate whether Nurr1 modulates the viability of A549 lung cancer cells by inducing mitochondrial dysfunction, with a focus on the p53-Drp1 signaling pathway.
methodswestern blotting, ELISA and immunofluorescence assay was used to verify the alterations of cell death. siRNA was used to determine the role of p53-Drp1 pathway in lung cancer death.
resultsNurr1 was downregulated in A549 lung cancer cells compared to normal pulmonary epithelial cells. Interestingly, overexpression of Nurr1 reduced the viability of A549 lung cancer cells by activating apoptosis and mitochondrial stress. At the molecular level, we provide data to support the regulatory effects of Nurr1 on the p53-Drp1 signaling pathway. Blockade of the p53-Drp1 signaling pathway abolished the proapoptotic action of Nurr1 on A549 cells and sustained mitochondrial homeostasis.
conclusionTaken together, our results depict the tumor-suppressive role played by Nurr1 in A549 lung cancer in vitro and show that the anticancer effects of Nurr1 are executed via triggering of mitochondrial dysfunction and activation of the p53-Drp1 signaling pathway.
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