ArticleCurrent cancer drug targets2011
A cross-talk between NFAT and NF-κB pathways is crucial for nickel-induced COX-2 expression in Beas-2B cells.
Article in Current cancer drug targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Redox sensitive miR-27a/b/Nrf2 signaling in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
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- PolyADP-Ribosylation of NFATc3 and NF-κB Transcription Factors Modulate Macrophage Inflammatory Gene Expression in LPS-Induced Acute Lung Injury.Journal of innate immunity · 2021Article
- Article
- Role of calcium channels and endothelial factors in nickel induced aortic hypercontraction in Wistar rats.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2018Article
- NFATc2 enhances tumor-initiating phenotypes through the NFATc2/SOX2/ALDH axis in lung adenocarcinoma.eLife · 2017Article
- Effect of Lead (Pb) on Inflammatory Processes in the Brain.International journal of molecular sciences · 2016Review
- Cheliensisin A (Chel A) induces apoptosis in human bladder cancer cells by promoting PHLPP2 protein degradation.Oncotarget · 2016Article
- Upregulation of SQSTM1/p62 contributes to nickel-induced malignant transformation of human bronchial epithelial cells.Autophagy · 2016Article
- NFATc4 Regulates Sox9 Gene Expression in Acinar Cell Plasticity and Pancreatic Cancer Initiation.Stem cells international · 2016Article
- Ethanol enhances arsenic-induced cyclooxygenase-2 expression via both NFAT and NF-κB signalings in colorectal cancer cells.Toxicology and applied pharmacology · 2015Article
- Article
- Nuclear factor of activated T-cell isoform expression and regulation in human myometrium.Reproductive biology and endocrinology : RB&E · 2015Article
- Inorganic Arsenic-induced cellular transformation is coupled with genome wide changes in chromatin structure, transcriptome and splicing patterns.BMC genomics · 2015Article
- Mechanism of Action of the Novel Nickel(II) Complex in Simultaneous Reactivation of the Apoptotic Signaling Networks Against Human Colon Cancer Cells.Frontiers in pharmacology · 2015Article
- Glaucomatous MYOC mutations activate the IL-1/NF-κB inflammatory stress response and the glaucoma marker SELE in trabecular meshwork cells.Molecular vision · 2015Article
- NFAT as cancer target: mission possible?Biochimica et biophysica acta · 2014Review
- Lead induces COX-2 expression in glial cells in a NFAT-dependent, AP-1/NFκB-independent manner.Toxicology · 2014Article
- c-Rel is a critical mediator of NF-κB-dependent TRAIL resistance of pancreatic cancer cells.Cell death & disease · 2014Article
- Isorhapontigenin (ISO) inhibited cell transformation by inducing G0/G1 phase arrest via increasing MKP-1 mRNA Stability.Oncotarget · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cyclooxygenase-2 (COX-2) is a critical enzyme implicated in chronic inflammation-associated cancer development. Our studies have shown that the exposure of Beas-2B cells, a human bronchial epithelial cell line, to lung carcinogenic nickel compounds results in increased COX-2 expression. However, the signaling pathways leading to nickel-induced COX-2 expression are not well understood. In the current study, we found that the exposure of Beas-2B cells to nickel compounds resulted in the activation of both nuclear factor of activated T cell (NFAT) and nuclear factor-κB (NF-κB). The expression of COX-2 induced upon nickel exposure was inhibited by either a NFAT pharmacological inhibitor or the knockdown of NFAT3 by specific siRNA. We further found that the activation of NFAT and NF-κB was dependent on each other. Since our previous studies have shown that NF-κB activation is critical for nickel-induced COX-2 expression in Beas-2B cells exposed to nickel compounds under same experimental condition, we anticipate that there might be a cross-talk between the activation of NFAT and NF-κB for the COX-2 induction due to nickel exposure in Beas-2B cells. Furthermore, we showed that the scavenging of reactive oxygen species (ROS) by introduction of mitochondrial catalase inhibited the activation of both NFAT and NF-κB, and the induction of COX-2 due to nickel exposure. Taken together, our results defining the evidence showing a key role of the cross-talk between NFAT and NF-κB pathways in regulating nickel-induced COX-2 expression, further provide insight into the understanding of the molecular mechanisms linking nickel exposure to its lung carcinogenic effects.
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