ArticleAge (Dordrecht, Netherlands)2016
Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21(waf-1).
Article in Age (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Soluble Epoxide Hydrolase Contributes to Cell Senescence and ER Stress in Aging Mice Colon.International journal of molecular sciences · 2023Article
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- Nutrition Interventions of Herbal Compounds on Cellular Senescence.Oxidative medicine and cellular longevity · 2022Review
- Review
- Article
- Single nucleotide polymorphisms (SNPs) in prostate cancer: its implications in diagnostics and therapeutics.American journal of translational research · 2021Review
- Review
- Natural Polyphenols Targeting Senescence: A Novel Prevention and Therapy Strategy for Cancer.International journal of molecular sciences · 2020Review
- Convergence of therapy-induced senescence (TIS) and EMT in multistep carcinogenesis: current opinions and emerging perspectives.Cell death discovery · 2020Review
- GSK-J4 induces cell cycle arrest and apoptosis via ER stress and the synergism between GSK-J4 and decitabine in acute myeloid leukemia KG-1a cells.Cancer cell international · 2020Article
- Review
- Article
- Dynamic recognition and repair of DNA complex damage.Journal of cellular physiology · 2019Article
- Regiospecific Synthesis of Ring A Fused Withaferin A Isoxazoline Analogues: Induction of Premature Senescence by W-2b in Proliferating Cancer Cells.Scientific reports · 2017Article
- Inhibition of Twist1-mediated invasion by Chk2 promotes premature senescence in p53-defective cancer cells.Cell death and differentiation · 2017Article
- AKT is indispensable for coordinating Par-4/JNK cross talk in p21 downmodulation during ER stress.Oncogenesis · 2017Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress-induced premature senescence (SIPS) is quite similar to replicative senescence that is committed by cells exposed to various stress conditions viz. ultraviolet radiation (DNA damage), hydrogen peroxide (oxidative stress), chemotherapeutic agents (cytotoxic threat), etc. Here, we report that cristacarpin, a natural product obtained from the stem bark of Erythrina suberosa, promotes endoplasmic reticulum (ER) stress, leading to sub-lethal reactive oxygen species (ROS) generation and which eventually terminates by triggering senescence in pancreatic and breast cancer cells through blocking the cell cycle in the G1 phase. The majority of cristacarpin-treated cells responded to conventional SA-β-gal stains; showed characteristic p21(waf1) upregulation along with enlarged and flattened morphology; and increased volume, granularity, and formation of heterochromatin foci-all of these features are the hallmarks of senescence. Inhibition of ROS generation by N-acetyl-L-cysteine (NAC) significantly reduced the expression of p21(waf1), confirming that the modulation in p21(waf1) by anti-proliferative cristacarpin was ROS dependent. Further, the elevation in p21(waf1) expression in PANC-1 and MCF-7 cells was consistent with the decrease in the expression of Cdk-2 and cyclinD1. Here, we provide evidence that cristacarpin promotes senescence in a p53-independent manner. Moreover, cristacarpin treatment induced p38MAPK, indicating the ROS-dependent activation of the MAP kinase pathway, and thus abrogates the tumor growth in mouse allograft tumor model.
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