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Gene expression profiling of transmitochondrial cybrids (triple negative breast cancer cells in SUM159 background)

ABSTRACT: We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72319 | GEO | 2016/04/14

SECONDARY ACCESSION(S): PRJNA293743

REPOSITORIES: GEO

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Gene expression profiling of transmitochondrial cybrids (triple negative breast cancer cells in SUM159 background)

Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids. SUM159 Ï0 cells were used as nuclear donor and A1N4 and SUM 159 cells were used as mitochondrial donor cells. The two groups were profiled for gene expression using microarrays. two group comparison (159/SUM159 vs A1/SUM159)

2016-04-14 | E-GEOD-72319 | biostudies-arrayexpress

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Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls. four samples with 12S rRNA hypermethylation (two cell lines, with two biological replicates each) versus four samples with basal 12S rRNA methylation (two cell lines, with two biological replicates each)

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Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

Project description:Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitochondria are inhibited in cybrids with non-cancerous mitochondria. These results suggest the critical oncogenic regulation by motochondrial-nuclear cross talk and highlights rectifying motochondiral functional properties as a promising target in cancer therapy.

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Project description:For many breast cancer (BCa) patients, symptomatic bone metastases appear after years or even decades of latency. How metastatic cells disseminate, and how micrometastatic lesions remain dormant and undetectable yet initiate colonization, are major questions in cancer research. Here we identify and functionally analyse a molecular mechanism involved in bone metastatic latency of estrogen receptor–positive (ER)+ BCa. We developed an in vivo loss-of-function, genome-wide shRNA screening to identify genes relevant for long-latent relapse in BCa. This screen revealed the kinase MSK1 as an important regulator of metastatic dormancy. Importantly, low MSK1 expression associates with early metastasis in ER+ BCa patients. Reduced MSK1 levels impaired cellular differentiation and increased the bone homing and growth capacity of metastatic cells. MSK1 modulates chromatin status at promoters to regulate the expression of luminal differentiation genes, including those for the GATA-3 and FOXA1 transcription factors, which prevent the progression of ER+ BCa towards metastasis. Our results identify the regulation of luminal cell differentiation by MSK1 via modulation of chromatin remodelling to be a key mechanism for controlling metastatic dormancy in BCa. We propose that MSK1 could be a useful marker for stratifying BCa patients as high- or low-risk for early relapse, allowing patients to receive appropriate treatments.

2017-11-13 | GSE100306 | GEO

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