ArticleThe Journal of biological chemistry2014
Receptor-interacting protein 1 increases chemoresistance by maintaining inhibitor of apoptosis protein levels and reducing reactive oxygen species through a microRNA-146a-mediated catalase pathway.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- Inflamma-miRs Profile in Myelodysplastic Syndrome Patients.International journal of molecular sciences · 2024Article
- Altered MicroRNA Maturation in Ischemic Hearts: Implication of Hypoxia on XPO5 and DICER1 Dysregulation and RedoximiR State.Antioxidants (Basel, Switzerland) · 2023Article
- Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential.Frontiers in pharmacology · 2023Review
- Receptor interacting protein 1 knockdown induces cell death in liver cancer by suppressing STAT3/ATR activation in a p53-dependent manner.American journal of cancer research · 2022Article
- IAP-1 promoted cisplatin resistance in nasopharyngeal carcinoma via inhibition of caspase-3-mediated apoptosis.American journal of cancer research · 2021Article
- RIP1 promotes proliferation through G2/M checkpoint progression and mediates cisplatin-induced apoptosis and necroptosis in human ovarian cancer cells.Acta pharmacologica Sinica · 2020Article
- Crosstalk between noncoding RNAs and ferroptosis: new dawn for overcoming cancer progression.Cell death & disease · 2020Review
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Metalloporphyrin Pd(T4) Exhibits Oncolytic Activity and Cumulative Effects with 5-ALA Photodynamic Treatment against C918 Cells.International journal of molecular sciences · 2020Article
- ERK Activation-Mediated Autophagy Induction Resists Licochalcone A-Induced Anticancer Activities in Lung Cancer CellsOncoTargets and therapy · 2020Article
- Crosstalk of MicroRNAs and Oxidative Stress in the Pathogenesis of Cancer.Oxidative medicine and cellular longevity · 2020Review
- The Yin-Yang Regulation of Reactive Oxygen Species and MicroRNAs in Cancer.International journal of molecular sciences · 2019Review
- CRTC2 promotes non-small cell lung cancer A549 migration and invasion in vitro.Thoracic cancer · 2018Article
- The Network of Non-coding RNAs in Cancer Drug Resistance.Frontiers in oncology · 2018Review
- RIPK1 binds to vitamin D receptor and decreases vitamin D-induced growth suppression.The Journal of steroid biochemistry and molecular biology · 2017Article
- Review
- Histone H4 expression is cooperatively maintained by IKKβ and Akt1 which attenuates cisplatin-induced apoptosis through the DNA-PK/RIP1/IAPs signaling cascade.Scientific reports · 2017Article
- MiR-491-5p negatively regulates cell proliferation and motility by targeting PDGFRA in prostate cancer.American journal of cancer research · 2017Article
- Klotho modulates FGF23-mediated NO synthesis and oxidative stress in human coronary artery endothelial cells.Pflugers Archiv : European journal of physiology · 2016Article
- Evaluation of RIP1K and RIP3K expressions in the malignant and benign breast tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Although receptor-interacting protein 1 (RIP1) is well known as a key mediator in cell survival and death signaling, whether RIP1 directly contributes to chemotherapy response in cancer has not been determined. In this report, we found that, in human lung cancer cells, knockdown of RIP1 substantially increased cytotoxicity induced by the frontline anticancer therapeutic drug cisplatin, which has been associated with robust cellular reactive oxygen species (ROS) accumulation and enhanced apoptosis. Scavenging ROS dramatically protected RIP1 knockdown cells against cisplatin-induced cytotoxicity. Furthermore, we found that, in RIP1 knockdown cells, the expression of the hydrogen peroxide-reducing enzyme catalase was dramatically reduced, which was associated with increased miR-146a expression. Inhibition of microRNA-146a restored catalase expression, suppressed ROS induction, and protected against cytotoxicity in cisplatin-treated RIP1 knockdown cells, suggesting that RIP1 maintains catalase expression to restrain ROS levels in therapy response in cancer cells. Additionally, cisplatin significantly triggered the proteasomal degradation of cellular inhibitor of apoptosis protein 1 and 2 (c-IAP1 and c-IAP2), and X-linked inhibitor of apoptosis (XIAP) in a ROS-dependent manner, and in RIP1 knockdown cells, ectopic expression of c-IAP2 attenuated cisplatin-induced cytotoxicity. Thus, our results establish a chemoresistant role for RIP1 that maintains inhibitor of apoptosis protein (IAP) expression by release of microRNA-146a-mediated catalase suppression, where intervention within this pathway may be exploited for chemosensitization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.