Non-microarray DNA differential methylation screening in breast cancer

Стрельников, В. В.; Танас, А. С.; Shkarupo, Viktoria; Кузнецова, Е. Б.; Горбань, Н. А.; Zaletaev, D. V.

doi:10.1016/j.cancergencyto.2010.07.103

Cited by 4 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The recent reports implicating TMEM176A or TMEM176B in human cancer were primarily based on data that show abnormal mRNA transcript levels for TMEM176A and/or 176B (Wang et al, 2002; Hodo et al, 2010; Ryu et al, 2010; Strelnikov et al, 2010; Gottschling et al, 2012). One caveat about these findings is that mRNA levels do not always positively correlate with protein levels in cells or tissues due to variables such as mRNA stability, translational regulation, or proteolysis.…”

Section: Resultsmentioning

confidence: 99%

“…Several reports have associated distinct types of human cancer with changes in tissue mRNA expression level or transcriptional regulation of TMEM176A and/or 176B genes (Wang et al, 2002; Hodo et al, 2010; Strelnikov et al, 2010; Gottschling et al, 2012) however, evidence that clearly shows abnormality of TMEM176A or 176B protein levels in these cancer tissues was lacking. In this study, we show that protein levels of both TMEM176A and 176B are significantly increased in lymphoma tissues, while TMEM176A protein alone is significantly elevated in lung carcinoma tissues (Table 2).…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal DNA methylation of CpG islands in human TMEM176A and 176B has been linked to breast cancer (Strelnikov et al, 2010). A study using serial analysis of gene expression showed that both 5′ and 3′ intronic transcripts encoding the human TMEM176B gene are significantly reduced in HCC tissues (Hodo et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology

et al. 2012

View full text Add to dashboard Cite

Transmembrane (TMEM)-176A and 176B proteins belong to the MS4A family of proteins whose function in the immune system remains unclear. TMEM176A transcripts were previously shown to be elevated in liver cancer or kidney tissue with proteinuria, while marked changes in TMEM176B transcripts have been found in tolerated tissue allografts and neoplastic fibroblasts. To study the functional relationship between human TMEM176A and 176B and their putative link to cancer, we used polymerase chain reaction and biochemical assays. Here, we show that TMEM176A and 176B are widely expressed in all human tissues examined. Co-immunoprecipitation of heterologously expressed TMEM176A and 176B revealed direct physical interaction. To determine the relevance of such interaction to cancer pathology, we analyzed biopsied tissue samples from a variety of normal and cancer tissues. Our data reveal that human TMEM176A and 176B protein levels are significantly elevated in lymphoma, but not in normal tissues. The protein levels of TMEM176A are also significantly increased in lung carcinoma. Finally, analysis of the protein expression ratio of TMEM176A over 176B showed significant differences between normal and cancer tissues of the breast, lymph, skin, and liver, which indicates that both TMEM proteins could be potential useful markers for certain human cancers.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology

et al. 2012

View full text Add to dashboard Cite

show abstract

“…(45,46) It was discovered in human lung fibroblasts and is associated with human small cell lung carcinoma. (47) Although several recent reports implicate human TMEM176B in cancer, (48)(49)(50) no direct evidence is available regarding its function in cancer pathogenesis, including tumor angiogenesis. Here, we report for the first time overexpression of TMEM176B in TEC and further show using RNAi that TMEM176B mediates TEC migration.…”

Section: Discussionmentioning

confidence: 99%

Identification of novel targets for antiangiogenic therapy by comparing the gene expressions of tumor and normal endothelial cells

et al. 2014

View full text Add to dashboard Cite

Targeting tumor angiogenesis is an established strategy for cancer therapy. Because angiogenesis is not limited to pathological conditions such as cancer, molecular markers that can distinguish between physiological and pathological angiogenesis are required to develop more effective and safer approaches for cancer treatment. To identify such molecules, we determined the gene expression profiles of murine tumor endothelial cells (mTEC) and murine normal endothelial cells using DNA microarray analysis followed by quantitative reverse transcription–polymerase chain reaction analysis. We identified 131 genes that were differentially upregulated in mTEC. Functional analysis using siRNA-mediated gene silencing revealed five novel tumor endothelial cell markers that were involved in the proliferation or migration of mTEC. The expression of DEF6 and TMEM176B was upregulated in tumor vessels of human renal cell carcinoma specimens, suggesting that they are potential targets for antiangiogenic intervention for renal cell carcinoma. Comparative gene expression analysis revealed molecular differences between tumor endothelial cells and normal endothelial cells and identified novel tumor endothelial cell markers that may be exploited to target tumor angiogenesis for cancer treatment.

show abstract

“…Abnormal methylation has been demonstrated for the genes involved in cell cycle regulation (CDKN2A, CDKN2B, p14/ARF, RB1, etc. ), apoptosis (TP53, CDKN1A, HOX5, MDM2, DAPK1, TWIST1, TMS1 and FHIT), invasion and metastasis (CDH1, CDH13 and CTNB), receptor mediated signaling (ESR1, PR and RARB) and many others [9][10][11][12][13][14][15].…”

mentioning

confidence: 99%

Genome-Wide Methylotyping Resolves Breast Cancer Epigenetic Heterogeneity and Suggests Novel Therapeutic Perspectives

et al. 2019

View full text Add to dashboard Cite

To provide a breast cancer (BC) methylotype classification by genome-wide CpG islands bisulfite DNA sequencing. Materials & methods: XmaI-reduced representation bisulfite sequencing DNA methylation sequencing method was used to profile DNA methylation of 110 BC samples and 6 normal breast samples. Intrinsic DNA methylation BC subtypes were elicited by unsupervised hierarchical cluster analysis, and cluster-specific differentially methylated genes were identified. Results & conclusion: Overall, six distinct BC methylotypes were identified. BC cell lines constitute a separate group extremely highly methylated at the CpG islands. In turn, primary BC samples segregate into two major subtypes, highly and moderately methylated. Highly and moderately methylated superclusters, each incorporate three distinct epigenomic BC clusters with specific features, suggesting novel perspectives for personalized therapy.

show abstract

Non-microarray DNA differential methylation screening in breast cancer

Cited by 4 publications

References 0 publications

Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology

Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology

Identification of novel targets for antiangiogenic therapy by comparing the gene expressions of tumor and normal endothelial cells

Genome-Wide Methylotyping Resolves Breast Cancer Epigenetic Heterogeneity and Suggests Novel Therapeutic Perspectives

Contact Info

Product

Resources

About