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Hypoxia response by human breast cancer cell MDA-MB-231 sublines

ABSTRACT: Two MDA-MB-231 sublines, SCP2 and LM2 (4175), were applied to low oxygen (1%) for 0, 6 and 24 hours, then profiled for RNA expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE17188 | GEO | 2010/06/07

SECONDARY ACCESSION(S): PRJNA119687

REPOSITORIES: GEO

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Hypoxia response by human breast cancer cell MDA-MB-231 sublines

Project description:Two MDA-MB-231 sublines, SCP2 and LM2 (4175), were applied to low oxygen (1%) for 0, 6 and 24 hours, then profiled for RNA expression. Two sublines, each sublines has three conditions: 0h, 6h and 24h for hypoxia treatment. Each condition has two repeats. Total 12 samples

2010-06-16 | E-GEOD-17188 | biostudies-arrayexpress

Next generation sequencing analysis of transcriptomes in MDA-MB-231 and LM2-4175 cell lines

Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the melecular mechanisms of lung metastasis in breast cancer,we analyzed the RNA-seq data of MDA-MB-231 and LM2-4175 cell lines.

2019-07-31 | GSE124380 | GEO

Genome-wide profiles of multiple histone modifications in MDA-MB-231 and LM2-4175 cell lines

Project description:LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the regulatory mechanisms of lung metastasis in breast cancer, we analyzed the chromatin structure of MDA-MB-231 and LM2-4175 cell lines.

2019-07-31 | GSE124379 | GEO

Enhancement of metastasis by spontaneous ploidy doubling of breast cancer cell MDA-MB-231.

Project description:MDA-MB-231 bone-metastatic subline 1833 and lung metastatic subline 4175 underwent spontaneous ploidy doubling in culture, i.e. the genome approximately duplicated itself gradually. The modal- and hyper-ploid subpopulations during the ploidy transition were sorted into two separate sublines, 1833-Modal and 1833-Hyper for 1833, 4175-Modal and 4175-Hyper for 4175. Their expresssion patterns were compared to each other as well as to other MDA-MB-231 sublines isolated previously by Kang et al. 2003 and Minn et al. 2005. Keywords: Cell type comparison 19 cell lines were analyzed, including the parental line MDA-MB-231, modal-ploid sublines 1833-Modal and 4175-Modal, hyper-ploid sublines 1833-Hyper and 4175-Hyper, strongly bone-metastatic lines 1833 (the original subline after short culture), 2274, 2268 and 2269, weakly bone-metastatic lines 2293, 2295 and 2297, strongly lung-metastaic lines 4142, 4173, 4175 (the original subline after short culture) and 4180, and weakly lung-metastatic lines SCP6, SCP21 and SCP26. Single sample for each line.

2010-06-08 | E-GEOD-16554 | biostudies-arrayexpress

Enhancement of metastasis by spontaneous ploidy doubling of breast cancer cell MDA-MB-231.

2010-06-01 | GSE16554 | GEO

Transcription profiling of human parental parental line MDA-MB-231 and fusion cell lines indicates hybrids assimilate organ-specific metastasis gene signatures from both parental cells

Project description:Spontaneous cell fusion of MDA-MB-231 bone-metastatic subline Bm (i.e., SCP2) and lung metastatic subline Lm (i.e., LM2) gave rise to hybrid lines BLm-FACS or BLm-DRUG, as well as its single clones (#8, #12, #18). The hybrids acquired the metastasis tropisms from both parental cells. Expression profiles of the parental cells, the hybrids and several previously characterized MDA-MB-231 metastatic derivatives were compared. Hierarchical clustering showed the hybrids assimilated the organ-specific metastasis gene signatures from both parental cells. Experiment Overall Design: Twenty-six cell lines were analyzed, including the parental line MDA-MB-231; cell fusion partner lines Bm and Lm; self-fused lines BBm and LLm; hetero-fused lines BLm-FACS, BLM-DRUG and clones BLm-DRUG-8, -12 and -18; strongly bone-metastatic lines 1833, SCP14, SCP20, SCP25 and SCP46; strongly lung-metastatic lines 3481, 4142, 4173, 4175 and 4180; and weakly metastatic lines SCP3, SCP4, SCP6, SCP28, SCP32 and SCP43. Single sample for each line.

2009-05-16 | E-GEOD-14244 | biostudies-arrayexpress

Hypoxia response by human breast cancer cell MDA-MB-231 sublines

| S-ECPF-GEOD-17188 | biostudies-other

Differential transcript stability measurements in MDA-MB-231 vs. MDA-LM2 cells

Project description:We performed whole-genome stability measurements for MDA-MB-231 and its highly metastatic derivative MDA-LM2. Our goal was to identify post-transcriptonal regulons that are deregulated en route to higher metastatic capacity.

2014-07-24 | GSE49608 | GEO

Next generation sequencing analysis of transcriptomes in MDA-MB-231 and LM2-4175 cell lines

Project description:Next generation sequencing analysis of transcriptomes in MDA-MB-231 and LM2-4175 cell lines

| PRJNA511878 | ENA

Sequencing of human breast cancer cell line MDA-MB-231 and its highly pulmonary metastatic subline MDA-MB-231-LM2

Project description:Purpose: Tumor metastasis is the main cause of death from breast cancer patients and cell migration plays a critical role in metastasis. Recent studies have shown long non-coding RNAs (lncRNAs) play an essential role in the initiation and progression of cancer. In the present study, the role of a LncRNA, Rho GTPase Activating Protein 5- Antisense 1 (ARHGAP5-AS1) in breast cancer was investigated. Methods: RNA sequencing was performed to find out dysregulated LncRNAs in MDA-MB-231-LM2 cells. Transwell migration assays and F-actin staining were utilized to estimate cell migration ability. RNA pulldown assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7. Western blot and immunofluorescence imaging were used to examine the protein levels. Dual luciferase reporter assays were performed to evaluate the activation of TGF-β signaling. Results: Compared to MDA-MB-231 cells, the expression of LncRNA ARHGAP5-AS1 (NR_027263) was significantly suppressed in its highly metastatic subtype MDA-MB-231-LM2 cells. Functional study showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. Moreover, ARHGAP5-AS1 could inhibit TGF-β signaling pathway due to its inhibitory role on SMAD7. Conclusion: Overall, these findings demonstrate that ARHGAP5-AS1 inhibits breast cancer cell migration and could serve as a novel biomarker for breast cancer metastasis and a potent target for the treatment in the future.

2021-05-20 | GSE174717 | GEO

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