In vitro model for gastroduodenal reflux-induced nuclear factor-kappaB activation and its role in hypopharyngeal carcinogenesis - PubMed (original) (raw)
. 2016 Apr:38 Suppl 1:E1381-91.
doi: 10.1002/hed.24231. Epub 2015 Nov 11.
Affiliations
- PMID: 26559497
- DOI: 10.1002/hed.24231
In vitro model for gastroduodenal reflux-induced nuclear factor-kappaB activation and its role in hypopharyngeal carcinogenesis
Clarence T Sasaki et al. Head Neck. 2016 Apr.
Abstract
Background: The purpose of this study was to investigate whether gastroduodenal reflux can play a role in the pathogenesis of hypopharyngeal cancer; therefore, we assessed its effect on the nuclear factor-kappa B (NF-κB) pathway, as similarly noted in the esophagus.
Methods: We exposed human cells derived from the hypopharyngeal epithelium to bile acids or deoxycholic acid. We centered our study on the transcriptional activation of NF-κB pathway, previously linked to head and neck squamous cell carcinoma (HNSCC).
Results: We show that acidic-bile salts induce: (1) NF-κB activation with high cytoplasmic Bcl-2 expression; (2) significant increase in expression v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA(p65)), v-rel avian reticuloendotheliosis viral oncogene homolog (c-REL) signal transducer and activator of transcription 3 (STAT3), isoform of transformation related protein p63 (ΔNp63), B-cell lymphoma 2 (Bcl-2), tumor necrosis factor alpha (TNF-α), epidermal growth factor receptor (EGFR), and wingless type MMTV integration site family member 5A (WNT5A) and a decrease in tumor protein p53 (Tp53); and (3) phenotypic changes that are similar to the phenotype of the untreated hypopharyngeal cancer cell line, University of Michigan squamous cell carcinoma (UMSCC)-11B. These changes are not seen when cells were exposed to neutral control or acid alone.
Conclusion: Our findings in vitro are consistent with the hypothesis that gastroduodenal reflux plays a role in hypopharyngeal carcinogenesis and its effect is mediated through activation of NF-κB pathway. © 2015 Wiley Periodicals, Inc. Head Neck 38: E1381-E1391, 2016.
Keywords: bile acids; gastroduodenal reflux; hypopharyngeal cancer; in vitro; nuclear factor-kappa B (NF-κB).
© 2015 Wiley Periodicals, Inc.
Similar articles
- Curcumin prevents the bile reflux-induced NF-κB-related mRNA oncogenic phenotype, in human hypopharyngeal cells.
Vageli DP, Doukas SG, Spock T, Sasaki CT. Vageli DP, et al. J Cell Mol Med. 2018 Sep;22(9):4209-4220. doi: 10.1111/jcmm.13701. Epub 2018 Jun 17. J Cell Mol Med. 2018. PMID: 29911313 Free PMC article. - Gastro-duodenal fluid induced nuclear factor-κappaB activation and early pre-malignant alterations in murine hypopharyngeal mucosa.
Vageli DP, Prasad ML, Sasaki CT. Vageli DP, et al. Oncotarget. 2016 Feb 2;7(5):5892-908. doi: 10.18632/oncotarget.6824. Oncotarget. 2016. PMID: 26745676 Free PMC article. - Biliary reflux as a causal factor in hypopharyngeal carcinoma: New clinical evidence and implications.
Sasaki CT, Doukas SG, Costa J, Vageli DP. Sasaki CT, et al. Cancer. 2019 Oct 15;125(20):3554-3565. doi: 10.1002/cncr.32369. Epub 2019 Jul 16. Cancer. 2019. PMID: 31310330 - Bile reflux and hypopharyngeal cancer (Review).
Vageli DP, Doukas SG, Doukas PG, Judson BL. Vageli DP, et al. Oncol Rep. 2021 Nov;46(5):244. doi: 10.3892/or.2021.8195. Epub 2021 Sep 24. Oncol Rep. 2021. PMID: 34558652 Free PMC article. Review. - Regulation of the MIR155 host gene in physiological and pathological processes.
Elton TS, Selemon H, Elton SM, Parinandi NL. Elton TS, et al. Gene. 2013 Dec 10;532(1):1-12. doi: 10.1016/j.gene.2012.12.009. Epub 2012 Dec 14. Gene. 2013. PMID: 23246696 Review.
Cited by
- NF-κB inhibition reverses acidic bile-induced miR-21, miR-155, miR-192, miR-34a, miR-375 and miR-451a deregulations in human hypopharyngeal cells.
Doukas SG, Vageli DP, Sasaki CT. Doukas SG, et al. J Cell Mol Med. 2018 May;22(5):2922-2934. doi: 10.1111/jcmm.13591. Epub 2018 Mar 8. J Cell Mol Med. 2018. PMID: 29516639 Free PMC article. - The in vivo preventive and therapeutic properties of curcumin in bile reflux-related oncogenesis of the hypopharynx.
Doukas SG, Doukas PG, Sasaki CT, Vageli D. Doukas SG, et al. J Cell Mol Med. 2020 Sep;24(18):10311-10321. doi: 10.1111/jcmm.15640. Epub 2020 Jul 21. J Cell Mol Med. 2020. PMID: 32691972 Free PMC article. - The temporal effects of topical NF-κB inhibition, in the in vivo prevention of bile-related oncogenic mRNA and miRNA phenotypes in murine hypopharyngeal mucosa: a preclinical model.
Vageli DP, Kasle D, Doukas SG, Doukas PG, Sasaki CT. Vageli DP, et al. Oncotarget. 2020 Sep 1;11(35):3303-3314. doi: 10.18632/oncotarget.27706. eCollection 2020 Sep 1. Oncotarget. 2020. PMID: 32934775 Free PMC article. - miR-21, miR-155, miR-192, and miR-375 Deregulations Related to NF-kappaB Activation in Gastroduodenal Fluid-Induced Early Preneoplastic Lesions of Laryngeal Mucosa In Vivo.
Sasaki CT, Vageli DP. Sasaki CT, et al. Neoplasia. 2016 Jun;18(6):329-38. doi: 10.1016/j.neo.2016.04.007. Epub 2016 May 25. Neoplasia. 2016. PMID: 27292022 Free PMC article. - Curcumin prevents the bile reflux-induced NF-κB-related mRNA oncogenic phenotype, in human hypopharyngeal cells.
Vageli DP, Doukas SG, Spock T, Sasaki CT. Vageli DP, et al. J Cell Mol Med. 2018 Sep;22(9):4209-4220. doi: 10.1111/jcmm.13701. Epub 2018 Jun 17. J Cell Mol Med. 2018. PMID: 29911313 Free PMC article.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous