Untitled

Nindl, Ingo; Dang, Chantip; Forschner, T.; Kuban, Ralf‐Jürgen; Meyer, Thomas; Sterry, Wolfram; Stockfleth, Eggert

doi:10.1186/1476-4598-5-30

Cited by 118 publications

(66 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, in our study, expression patterns detected in MM prone cells from non-lesional areas of the skin were compared with those observed in skin cancer tumors (SCCs and CMs) [35, 36]. Although differences in the experimental designs among studies (normal skin cells vs tumoral tissue or cultured cells vs fresh-frozen tissue) may interfere in the analysis, the expression patterns detected in our study correlate to those observed in skin tumors.…”

Section: Discussionmentioning

confidence: 52%

“…To support our hypothesis, the expression pattern of the most deregulated genes in mutant CDKN2A or RHC MC1R variant skin cells was compared to their expression observed in two previously published skin cancer datasets. The GSE2503 dataset contained the whole genome expression of five squamous cell carcinomas (SCCs) and six healthy skin samples[35] and the GSE12391 dataset included 23 melanomas (CMs) at different stages (radial growth phase or vertical growth phase) and 18 common nevi[36]. Due to differences in the array platforms used among the studies, only the expression of genes present in all datasets was evaluated (Figure 5).…”

Section: Resultsmentioning

confidence: 99%

“…In order to gain insight into the co-regulation patterns on transcript expression profiles, data from our microarray experiments were clustered together with expression data obtained from two previous experiments focused on NMSC (GSE2503 dataset[35]) and MM (GSE12391 dataset[36]). Raw data were obtained from the Gene Expression Omnibus.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Capturing the biological impact of CDKN2A and MC1R genes as an early predisposing event in melanoma and non melanoma skin cancer

et al. 2013

View full text Add to dashboard Cite

Germline mutations in CDKN2A and/or red hair color variants in MC1R genes are associated with an increased susceptibility to develop cutaneous melanoma or non melanoma skin cancer.We studied the impact of the CDKN2A germinal mutation p.G101W and MC1R variants on gene expression and transcription profiles associated with skin cancer. To this end we set-up primary skin cell co-cultures from siblings of melanoma prone-families that were later analyzed using the expression array approach.As a result, we found that 1535 transcripts were deregulated in CDKN2A mutated cells, with over-expression of immunity-related genes (HLA-DPB1, CLEC2B, IFI44, IFI44L, IFI27, IFIT1, IFIT2, SP110 and IFNK) and down-regulation of genes playing a role in the Notch signaling pathway. 3570 transcripts were deregulated in MC1R variant carriers. In particular, genes related to oxidative stress and DNA damage pathways were up-regulated as well as genes associated with neurodegenerative diseases such as Parkinson’s, Alzheimer and Huntington.Finally, we observed that the expression signatures indentified in phenotypically normal cells carrying CDKN2A mutations or MC1R variants are maintained in skin cancer tumors (melanoma and squamous cell carcinoma). These results indicate that transcriptome deregulation represents an early event critical for skin cancer development.

show abstract

Section: Discussionmentioning

confidence: 52%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Capturing the biological impact of CDKN2A and MC1R genes as an early predisposing event in melanoma and non melanoma skin cancer

et al. 2013

View full text Add to dashboard Cite

show abstract

“…SphK1 is also overexpressed in acute leukemia patients [15]. Analyses of microarray data available online (http://www.oncomine.org/, http://www.ncbi.nlm.nih.gov/geo/) show statistically significant increases in SphK1 expression in: N-methyl-N-nitrosourea-induced rat breast cancer model [16]; recurrent breast cancer following tamoxifen therapy [17]; squamous cell carcinoma and it’s precursor actinic keratotic lesions in non-melanoma [18] and melanoma skin cancers [19]; advanced stages of cervical cancer [20]; invasive carcinoma of bladder [21]; oligodendrogliomas [22]; head and neck cancer [23,24]; leukemia, including B- and T-cell acute lymphoblastic leukemia and acute myeloid leukemia [25]; and in adult male germ cell tumors [26] (Fig. 1 ).…”

Section: Sphk1: Expression Activation and Translocationmentioning

confidence: 99%

Targeting SphK1 as a New Strategy against Cancer

Shida¹,

Takabe²,

Kapitonov³

et al. 2008

CDT

282

280

View full text Add to dashboard Cite

Sphingolipid metabolites have emerged as critical players in a number of fundamental biological processes. Among them, sphingosine-1-phosphate (S1P) promotes cell survival and proliferation, in contrast to ceramide and sphingosine, which induce cell growth arrest and apoptosis. These sphingolipids with opposing functions are interconvertible inside cells, suggesting that a finely tuned balance between them can determine cell fate. Sphingosine kinases (SphKs), which catalyze the phosphorylation of sphingosine to S1P, are critical regulators of this balance. Of the two identified SphKs, sphingosine kinase type 1 (SphK1) has been shown to regulate various processes important for cancer progression and will be the focus of this review, since much less is known of biological functions of SphK2, especially in cancer. SphK1 is overexpressed in various types of cancers and upregulation of SphK1 has been associated with tumor angiogenesis and resistance to radiation and chemotherapy. Many growth factors, through their tyrosine kinase receptors (RTKs), stimulate SphK1 leading to a rapid increase in S1P. This S1P in turn can activate S1P receptors and their downstream signaling. Conversely, activation of S1P receptors can induce transactivation of various RTKs. Thus, SphK1 may play important roles in S1P receptor RTK amplification loops. Here we review the role of SphK1 in tumorigenesis, hormonal therapy, chemotherapy resistance, and as a prognostic marker. We will also review studies on the effects of SphK inhibitors in cells in vitro and in animals in vivo and in some clinical trials and highlight the potential of SphK1 as a new target for cancer therapeutics.

show abstract

“…( B ) levels of MTA1 and DNMT3a in cancer cells when compared to the normal cells in Oncomine Cancer Profiling Database. Box’s detail: 1, 10, gastric3940; 2, anaplastic oligodendroglioma41; 3, renal cell carcinoma42, 4–5, Ovarian cell carcinoma43; 6–7, Skin4445 and 8–9, colon cancers46 TCGA Colorectal, 2011]. The p-value is provided for the medium-rank analysis.…”

Section: Figurementioning

confidence: 99%

Metastasis-associated protein 1 is an upstream regulator of DNMT3a and stimulator of insulin-growth factor binding protein-3 in breast cancer

Deivendran

Marzook

Santhoshkumar

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Despite a recognized role of DNA methyltransferase 3a (DNMT3a) in human cancer, the nature of its upstream regulator(s) and relationship with the master chromatin remodeling factor MTA1, continues to be poorly understood. Here, we found an inverse relationship between the levels of MTA1 and DNMT3a in human cancer and that high levels of MTA1 in combination of low DNMT3a status correlates well with poor survival of breast cancer patients. We discovered that MTA1 represses DNMT3a expression via HDAC1/YY1 transcription factor complex. Because IGFBP3 is an established target of DNMT3a, we investigated the effect of MTA1 upon IGFBP3 expression, and found a coactivator role of MTA1/c-Jun/Pol II coactivator complex upon the IGFBP3 transcription. In addition, MTA1 overexpression correlates well with low levels of DNMT3a which, in turn also correlates with a high IGFBP3 status in breast cancer patients and predicts a poor clinical outcome for breast cancer patients. These findings suggest that MTA1 could regulate the expression of IGFBP3 in both DNMT3a-dependent and -independent manner. Together findings presented here recognize an inherent role of MTA1 as a modifier of DNMT3a and IGFBP3 expression, and consequently, the role of MTA1-DNMT3a-IGFBP3 axis in breast cancer progression.

show abstract

Untitled

Abstract: Background: Carcinogenesis is a multi-step process indicated by several genes up-or downregulated during tumor progression. This study examined and identified differentially expressed genes in cutaneous squamous cell carcinoma (SCC).

Cited by 118 publications

References 43 publications

Capturing the biological impact of CDKN2A and MC1R genes as an early predisposing event in melanoma and non melanoma skin cancer

Capturing the biological impact of CDKN2A and MC1R genes as an early predisposing event in melanoma and non melanoma skin cancer

Targeting SphK1 as a New Strategy against Cancer

Metastasis-associated protein 1 is an upstream regulator of DNMT3a and stimulator of insulin-growth factor binding protein-3 in breast cancer

Contact Info

Product

Resources

About