Expression profiling of cancer-related genes in human keratinocytes following non-lethal ultraviolet B irradiation

Murakami, Takashi; Fujimoto, Manato; Ohtsuki, Mamitaro; Nakagawa, Hidemi

doi:10.1016/s0923-1811(01)00124-4

Cited by 70 publications

(57 citation statements)

References 48 publications

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“…After establishing the huCOP1 silenced transgenic keratinocyte cell line, we examined the expression of selected UVB-regulated genes with or without UVB irrradiation. Our experiments revealed that (i) the silencing of huCOP1 did not affect cell viability, (ii) the expression level of the selected genes was not affected by huCOP1 silencing in unirradiated cells, and (iii) DNA array and validating real-time RT-PCR experiments confirmed that transcript levels of the selected genes exhibited changes as early as 2 hours after UVB irradiation and that these changes were in good agreement with previously published data [1][2][3][4]. However, very importantly, we found that (i) the residual huCOP1 level was further reduced by UVB and (ii) the significantly reduced huCOP1 level resulted in more pronounced UVB-induced changes in the expression of genes as compared to nontransgenic keratinocytes.…”

Section: Discussionsupporting

confidence: 91%

“…We choose three upstream regulator molecules (IL1B, IL6 and NFKB) to test wheather the corresponding genes exhibit UVB-induced changes in expression. In agreement with published data [2,4,23], our results demonstrated that the transcription of these genes is UVB sensitive and that huCOP1 silencing had an effect on their transcription levels after UVB irradiation (Fig. 5b).…”

Section: A Uvb Regulatory Network Identified By Pathway Analysis Was supporting

confidence: 93%

“…UVB irradiation changes the expression of several genes in keratinocytes, including the p53 nuclear phosphoprotein [1][2][3]. This tumor suppressor functions as a transcription factor and has a central role in keratinocyte stress responses, including UV-induced responses [1][2][3][4][5]. The UVB-dependent molecular network in which p53 plays a pivotal role has not been revealed yet.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

UVB-dependent changes in the expression of fast-responding early genes is modulated by huCOP1 in keratinocytes

Fazekas

Polyánka

Bebes

et al. 2014

Journal of Photochemistry and Photobiology B: Biology

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Ultraviolet (UV) B is the most prominent physical carcinogen in the environment leading to the development of various skin cancers. We have previously demonstrated that the human ortholog of the Arabidopsis thaliana constitutive photomorphogenesis 1 (COP1) protein, huCOP1, is expressed in keratinocytes in a UVB-regulated manner and is a negative regulator of p53 as a posttranslational modifier. However, it was not known whether huCOP1 plays a role in mediating the UVB-induced early transcriptional responses of human keratinocytes. In this study, we report that stable siRNA-mediated silencing of huCOP1 affects the UVB response of several genes within 2 h of irradiation, indicating that altered huCOP1 expression sensitizes the cells toward UVB.Pathway analysis identified a molecular network in which 13 of the 30 examined UVB-regulated genes were organized around three central proteins. Since the expression of the investigated genes was upregulated by UVB in the siCOP1 cell line, we hypothesize that huCOP1 is a repressor of the identified pathway. Several members of the network have been implicated previously in the pathogenesis of non-melanoma skin cancers; therefore, clarifying the role of huCOP1 in these skin diseases may have clinical relevance in the future.

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Section: Discussionsupporting

confidence: 91%

Section: A Uvb Regulatory Network Identified By Pathway Analysis Was supporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

UVB-dependent changes in the expression of fast-responding early genes is modulated by huCOP1 in keratinocytes

Fazekas

Polyánka

Bebes

et al. 2014

Journal of Photochemistry and Photobiology B: Biology

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“…[22][23] RhoE, as an important component of the signaling pathways, its expression is highly regulated transcriptionally and a variety of studies using microarray analyses have suggested that RhoE mRNA can be altered under various physiological and pathological conditions. [25][26][27][28][29] Here we found that expression of RhoE mRNA was significantly associated with RhoE gene copy number changes (p < 0.05). Nearly all the cases (12/13) with overexpressed RhoE mRNA had copy number changes except one with the relative copy number near to the cut-off value (1.43 vs. 1.5).…”

Section: Discussionmentioning

confidence: 98%

Overexpression of RhoE in non-small cell lung cancer (NSCLC) is associated with smoking and correlates with DNA copy number changes

Zhang¹,

Hu²,

Zhou³

et al. 2007

Cancer Biology & Therapy

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RhoE, a small G protein, is constitutively GTP bound within the cell and can regulate actin cytoskeleton reorganization, leading to the appearance of aggregates of actin filaments. Although emerging evidence suggests that RhoE is causally involved in cancer formation and progression, little is known about its significance in solid cancer, including lung cancer. In the present study, the expression of RhoE was analyzed using Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR), real-time RT-PCR, immunohistochemistry and western blot in 30 patients with Non-small Cell Lung Cancer (NSCLC). Then the correlation of RhoE overexpression with clinical parameters was evaluated. Furthermore, the possible reasons contributing to the RhoE expression were examined by real-time genomic PCR and mutation analysis on DNA sequence and cDNA sequence. Our results revealed that RhoE expression was dramatically increased in lung cancer tissues compared with adjacent nontumoral lung tissues (p < 0.01). Immunohistochemistry showed a strong cytoplasmic staining in cancer cells compared with positive membrane staining in adjacent nontumoral proliferative alveolar epitheliums. Moreover, the overexpression of RhoE was significantly associated with the patients' smoking history (p < 0.05). 72% tumor tissues displayed DNA copy number changes based on the DNA levels in the matched adjacent nontumoral lung tissues and this copy number changes correlated significantly with RhoE expression and smoking history (p < 0.05). Three polymorphisms were identified but no correlation was found with the clinicopathological features. To our knowledge, this is the first report demonstrating that overexpression of RhoE correlated with smoking and DNA copy number changes, suggesting that RhoE may serve as a molecular marker to identify high-risk individuals and assist in the identification of additional pathways of carcinogenesis.

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“…DNA microarray technology has become a useful tool for the evaluation of global gene expression in UV-damaged cells. Several microarray analyses of UV-B-irradiated keratinocytes have yielded similar, almost identical, results in spite of considerable difference in experimental conditions [14][15][16][17] . Several papers on the microarray analysis of UV-B irradiated melanocytes, another cellular component of the epidermis, have also been published [18][19][20] .…”

mentioning

confidence: 87%

Mitotic genes are transcriptionally upregulated in the fibroblast irradiated with very low doses of UV-C

Takeuchi

Matsuda

Ono

et al. 2017

Journal of Dermatological Science

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Expression profiling of cancer-related genes in human keratinocytes following non-lethal ultraviolet B irradiation

Cited by 70 publications

References 48 publications

UVB-dependent changes in the expression of fast-responding early genes is modulated by huCOP1 in keratinocytes

UVB-dependent changes in the expression of fast-responding early genes is modulated by huCOP1 in keratinocytes

Overexpression of RhoE in non-small cell lung cancer (NSCLC) is associated with smoking and correlates with DNA copy number changes

Mitotic genes are transcriptionally upregulated in the fibroblast irradiated with very low doses of UV-C

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