Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short‐term exposure to tobacco smoke

Niimori-Kita, Kanako; Ogino, Kiyoshi; Mikami, Sayaka; Kudoh, Shinji; Koizumi, Daikai; Kudoh, Noritaka; Nakamura, Fumiko; Misumi, Masahiro; Shimomura, Taizo; Hasegawa, Koki; Usui, Fumihiko; Nagahara, Noriyuki; Ito, Takaaki

doi:10.1016/j.fob.2014.08.002

Cited by 11 publications

(8 citation statements)

References 65 publications

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“…It has been reported that the transcription factor (TF) STAT can be activated after tobacco smoke exposure. 46 Functional prediction analysis from HaploReg showed that rs3769201 had a STAT binding site motif, and the results of eQTL in the present study also demonstrated that the SNP may alter the mRNA expression of ZAK. However, there is no significant difference between ever smokers and never smokers as tested by the heterogeneity test.…”

Section: Discussionsupporting

confidence: 72%

“…Cigarette smoke is the major risk factor for lung cancer, especially for SC. It has been reported that the transcription factor (TF) STAT can be activated after tobacco smoke exposure . Functional prediction analysis from HaploReg showed that rs3769201 had a STAT binding site motif, and the results of eQTL in the present study also demonstrated that the SNP may alter the mRNA expression of ZAK .…”

Section: Discussionsupporting

confidence: 64%

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Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer

Feng

Wang

Liu

et al. 2017

Molecular Carcinogenesis

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The P38MAPK pathway participates in regulating cell cycle, inflammation, development, cell death, cell differentiation, and tumorigenesis. Genetic variants of some genes in the P38MAPK pathway are reportedly associated with lung cancer risk. To substantiate this finding, we used six genome-wide association studies (GWASs) to comprehensively investigate associations of 14,904 single nucleotide polymorphisms (SNPs) in 108 genes of this pathway with lung cancer risk. We identified six significant lung cancer risk-associated SNPs in two genes (CSNK2B and ZAK) after correction for multiple comparisons by a false discovery rate (FDR) < 0.20. After removal of three CSNK2B SNPs that are located on the same locus previously reported GWAS, we performed LD analysis, SNP functional prediction and further analysis for two independent SNPs: rs3769201 and rs722864 in ZAK. We also expanded the analysis by including these two SNPs from additional GWAS datasets of Harvard University (984 cases and 970 controls) and deCODE (1,319 cases and 26,380 controls). The overall effects of these two SNPs were assessed using all eight GWAS datasets (OR=0.92, 95% CI=0.89–0.95, and P=1.03E-05 for rs3769201; OR=0.91, 95% CI=0.88–0.95, and P=2.03E-06 for rs722864). Finally, we performed an eQTL analysis and found that these two SNPs were significantly associated with ZAK mRNA expression levels in lymphoblastoid cell lines. In conclusion, the ZAK rs3769201 and rs722864 may be possible functional susceptibility loci for lung cancer risk.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionsupporting

confidence: 64%

Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer

Feng

Wang

Liu

et al. 2017

Molecular Carcinogenesis

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“…The 2D-DIGE method is a useful tool to reveal functional post-translational modifications of nuclear factors that cannot be detected with DNA microarray. A shotgun proteome approach using nano-liquid chromatography (nanoLC) tandem mass spectrometry incorporating phosphopeptide enrichment can detect phosphorylated peptides in a highly sensitive manner 32 . However, proteomics analysis using 2D-DIGE can clearly indicate the molecular weight and pH of proteins in 2D-electrophoresis, provides more credible results concerning nuclear protein identification, and displays better quantitative reproducibility.…”

Section: Discussionmentioning

confidence: 99%

Matrin-3 is essential for fibroblast growth factor 2-dependent maintenance of neural stem cells

Niimori-Kita

Tamamaki

Koizumi

et al. 2018

Sci Rep

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To investigate the mechanisms underlying the maintenance of neural stem cells, we performed two-dimensional fluorescence-difference gel electrophoresis (2D-DIGE) targeting the nuclear phosphorylated proteins. Nuclear phosphorylated protein Matrin-3 was identified in neural stem cells (NSCs) after stimulation using fibroblast growth factor 2 (FGF2). Matrin-3 was expressed in the mouse embryonic subventricular and ventricular zones. Small interfering RNA (siRNA)-mediated knockdown of Matrin-3 caused neuronal differentiation of NSCs in vitro, and altered the cerebral layer structure of foetal brain in vivo. Transfection of Matrin-3 plasmids in which the serine 208 residue was point-mutated to alanine (Ser208Ala mutant Matrin3) and inhibition of Ataxia telangiectasia mutated kinase (ATM kinase), which phosphorylates Matrin-3 Ser208 residue, caused neuronal differentiation and decreased the proliferation of neurosphere-forming stem cells. Thus, our proteomic approach revealed that Matrin-3 phosphorylation was essential for FGF2-dependent maintenance of NSCs in vitro and in vivo.

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“…Nicotine can induce cell proliferation, invasion, and metastasis in several cancers [27, 28]. Nicotine-induced Prx1 overexpression correlates significantly with OSCC carcinogenesis [12, 29], and further investigation of the functional role of Prx1 could provide a novel biomarker for OSCC prevention and therapy.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis

et al. 2016

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Tobacco smoking is the major risk factor for oral squamous cell carcinoma (OSCC). Previously, we found that nicotine up-regulates peroxiredoxin 1 (Prx1), an important antioxidant enzyme, and nuclear factor kappa B (NFκB) in OSCC cells. However, the molecular mechanism of Prx1 in oral carcinogenesis remains obscure. To improve our understanding of the functional role of Prx1 during the cascade of tobacco-associated oral carcinogenesis, we characterized Prx1, NFκB, and epithelial-to-mesenchymal transition (EMT) markers including E-cadherin, vimentin and Snail in 30 primary oral tumors (15 from smokers with OSCC and 15 from non-smokers with OSCC) and 10 normal oral mucosa specimens from healthy individuals. The expression levels of Prx1, nuclear NFκB, vimentin and Snail were higher in the tumors from smokers with OSCC than in those from non-smokers with OSCC or the healthy controls. The expression levels of E-cadherin showed an opposite trend. Prx1 silencing suppressed the nicotine-induced EMT, cell invasion and migration in SCC15 cells in vitro. Furthermore, Prx1 activated the NFκB pathway in SCC15 cells. Prx1 might therefore play an oncogenic role in tobacco-related OSCC and thus serve as a target for chemopreventive and therapeutic interventions.

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Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short‐term exposure to tobacco smoke

Abstract: Graphical abstract

Cited by 11 publications

References 65 publications

Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer

Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer

Matrin-3 is essential for fibroblast growth factor 2-dependent maintenance of neural stem cells

Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis

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