ArticleEnvironmental health perspectives2010
mot-2-Mediated cross talk between nuclear factor-B and p53 is involved in arsenite-induced tumorigenesis of human embryo lung fibroblast cells.
Article in Environmental health perspectives, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 28 citations in OpenAlex.
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- NF-κB p65 promotes ovarian cancer cell proliferation and migration via regulating mortalin.Journal of cellular and molecular medicine · 2019Article
- Arsenic trioxide reverses the chemoresistance in hepatocellular carcinoma: a targeted intervention of 14-3-3η/NF-κB feedback loop.Journal of experimental & clinical cancer research : CR · 2018Article
- Inactivation of miR-100 combined with arsenic treatment enhances the malignant transformation of BEAS-2B cells via stimulating epithelial -mesenchymal transition.Cancer biology & therapy · 2017Article
- Article
- Feedback regulations of miR-21 and MAPKs via Pdcd4 and Spry1 are involved in arsenite-induced cell malignant transformation.PloS one · 2013Article
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9 authors at 1 institution in 1 country.
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Abstract
backgroundInactivation of p53 is involved in arsenite-induced tumorigenesis; however, the molecular mechanisms remain poorly understood.
objectiveWe investigated the molecular mechanisms underlying the inactivation of p53 and neoplastic transformation induced by arsenite in human embryo lung fibroblast (HELF) cells.
methodsAnchorage-independent growth assays were performed, and tumorigenicity in intact animals was assessed to confirm arsenite-induced neoplastic transformation. We determined the levels and functions of p53, nuclear factor-kappa B (NF-B; a key transcriptional regulator), and mot-2 (a p53 inhibitor) and their relationships in arsenite-induced transformed HELF cells by two-dimensional electrophoresis, reverse-transcriptase polymerase chain reaction, Western blot, immunofluorescence, and co-immunoprecipitation assays.
resultsExposure of HELF cells to low levels of arsenite increased their proliferation rate and anchorage-independent growth and disrupted normal contact inhibition. When introduced into nude mice, transformed cells were tumorigenic. We used proteomic analysis to identify proteins with altered expression between untreated and arsenite-exposed cells. We found decreased expression of NF-B repressing factor (NKRF; an inhibitor of NF-B-mediated gene transcription), increased expression of mot-2, and increased activation of NF-B. Changes in cells exposed to 1.0 microM arsenite were more marked than changes in cells exposed to 0.5 or 2.0 microM arsenite. Inactivation of NF-B prevented malignant transformation induced by 1.0 microM arsenite. Moreover, we also identified a mechanism whereby NF-B regulated p53. Specifically, activation of NF-B up-regulated mot-2 expression, which prevented nuclear translocation of p53 and switched the binding preference of the p53 and NF-B coactivator CBP [cyclic AMP-responsive element binding protein (CREB) binding protein] from p53 to NF-B.
conclusionsmot-2-mediated cross talk between NF-B and p53 appears to be involved in arsenite-induced tumorigenesis of HELF cells.
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