Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA expression profiling in diffuse malignant peritoneal mesothelioma

ABSTRACT: Diffuse malignant peritoneal mesothelioma (DMPM) is a rapidly lethal malignancy. The comprehension of the molecular and cellular features of DMPM is of utmost importance for the fruitful management of the disease, especially in patients who fail standard treatments and have a poor prognosis due to the lack of effective alternative therapeutic options. In this context, we previously found that telomerase activity (TA), which accounts for the limitless proliferative potential of cancer cells, is prognostic for disease relapse and cancer-related death in DMPM patients. Consequently, the identification of factors involved in telomerase activation/regulation may pave the way towards the development of novel therapeutic interventions for the disease. In the present study, miRNA expression profiling was carried out in a series of DMPM tissue specimens, previously characterized for the occurrence of TA, in order to possibly identify miRNAs that may play a role in the establishment/regulation of such a telomere maintenance mechanism in this malignancy and consequently furnish a biological rationale for the possible future development of miRNA-based telomerase-targeted therapeutic approaches.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99362 | GEO | 2017/08/11

SECONDARY ACCESSION(S): PRJNA388196

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of diffuse malignant peritoneal mesothelioma

Project description:Diffuse malignant peritoneal mesothelioma (DMPM) is a rapidly lethal malignancy. The comprehension of the molecular features of DMPM is of utmost importance for the fruitful management of the disease, especially in patients who fail standard treatments and have a poor prognosis due to the lack of effective alternative therapeutic options.

2019-02-07 | GSE112154 | GEO

Transcriptome profiling of mesothelioma cell lines

Project description:Malignant pleural mesothelioma (MPM) is characterized by dismal prognosis. Consequently, dissection of the molecular mechanisms driving malignancy is of key importance. Here we investigate whether activating mutations in the telomerase reverse transcriptase (TERT) gene promoter are present in MPM and associated with disease progression, cell immortalization, and genomic alteration patterns.

2020-05-01 | E-MTAB-8986 | biostudies-arrayexpress

ArrayCGH of Mesothelioma Cell Lines

2020-05-01 | E-MTAB-8987 | biostudies-arrayexpress

Whole Genome Sequencing of Mesothelioma Cell Lines

2020-05-03 | E-MTAB-8989 | biostudies-arrayexpress

Expression data by telomere elongation

Project description:Limitless reproductive potential is one of the hallmarks of cancer cells1. This ability is accomplished by maintaining telomeres, which erosion otherwise causes cellular senescence or death. Human cancer cells often maintain shorter telomeres than do cells in surrounding normal tissues2-5. While most cancer cells activate telomerase, which can elongate telomeres6, it remains elusive why cancer cells keep telomeres short. Here we show that forced elongation of telomeres in cancer cells promotes their differentiation in a tumor microenvironment in vivo. We elongated telomeres of human prostate cancer PC-3 cells, which possess short telomeres7, by enhancing their telomerase activity. The resulting cells with long telomeres retain an ability to form tumors in a mouse xenograft model. Strikingly, these tumors exhibit many duct-like structures and reduced N-cadherin expression, reminiscent of well-differentiated adenocarcinoma. These phenotypic changes are caused by telomere elongation per se but not enhanced telomerase activity. Gene expression profiling revealed that telomere elongation correlates with inhibition of cell-cycle processes. Together, our results suggest a functional contribution of short telomeres to tumor malignancy by regulating cancer cell differentiation. Two samples are telomere-elongated cells, both in the presence and absence of the exogenous hTERT. The other two samples are control cell lines.

2013-05-31 | E-GEOD-36649 | biostudies-arrayexpress

Expression data by telomere elongation in vivo (xenograft)

Project description:Limitless reproductive potential is one of the hallmarks of cancer cells1. This ability is accomplished by maintaining telomeres, which erosion otherwise causes cellular senescence or death. Human cancer cells often maintain shorter telomeres than do cells in surrounding normal tissues2-5. While most cancer cells activate telomerase, which can elongate telomeres6, it remains elusive why cancer cells keep telomeres short. Here we show that forced elongation of telomeres in cancer cells promotes their differentiation in a tumor microenvironment in vivo. We elongated telomeres of human prostate cancer PC-3 cells, which possess short telomeres7, by enhancing their telomerase activity. The resulting cells with long telomeres retain an ability to form tumors in a mouse xenograft model. Strikingly, these tumors exhibit many duct-like structures and reduced N-cadherin expression, reminiscent of well-differentiated adenocarcinoma. These phenotypic changes are caused by telomere elongation per se but not enhanced telomerase activity. Gene expression profiling revealed that telomere elongation correlates with inhibition of cell-cycle processes. Together, our results suggest a functional contribution of short telomeres to tumor malignancy by regulating cancer cell differentiation. Two cell lines are telomere-elongated cells, both in the presence and absence of the exogenous hTERT. The other two lines are control PC-3 cell lines. We extracted RNA from four independent xenograft tumors per original cell line.

2013-05-31 | E-GEOD-41559 | biostudies-arrayexpress

Expression data by telomere elongation in vivo (xenograft)

2013-05-31 | GSE41559 | GEO

Expression data by telomere elongation

2013-05-31 | GSE36649 | GEO

Regulation of hTERT by BCR-ABL at multiple levels in K562 cells

Project description:To investigate the mechanism of telomerase regulation in BCR-ABL positive cells due to its clinical value, we studied the catalytic component of telomerase, TERT. Our results suggest that BCR-ABL plays an important role in regulating hTERT in K562 (BCR-ABL positive human leukemia) cells. When Gleevec inhibited the tyrosine kinase activity of BCR-ABL, phosphorylation of hTERT was downregulated, therefore suggesting a positive correlation between BCR-ABL and hTERT. Gleevec treatment inhibited hTERT at the mRNA level and significantly reduced telomerase activity (TA) in K562 cells, but not in HL60 or Jurkat cells. TRAP assay also revealed that Gleevec treatment significantly reduced TA specifically in K562 cells. Furthermore, translocation of hTERT from nucleoli to nucleoplasm was observed in K562 cells induced by Gleevec. Although Gleevec down-regulated hTERT mRNA level, the protein level of hTERT remained unchanged. Therefore, Gleevec-induced-TA decrease is not due to the alteration in telomerase subunits expression. It could be presumably due to posttranslational modification of hTERT, possibly through multiple signaling pathways. We have found that Gleevec reduced the tyrosine phosphorylation of hTERT by BCR-ABL, which is associated with the nucleoplasm localization of hTERT from nucleoli sequesters. These findings reveal unknown functions and regulations of telomerase by BCR-ABL.

2011-12-15 | GSE26821 | GEO

Regulation of hTERT by BCR-ABL at multiple levels in K562 cells

2011-12-15 | E-GEOD-26821 | biostudies-arrayexpress