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

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

PROVIDER: PRJNA511878 | ENA |

REPOSITORIES: ENA

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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

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

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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.

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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. Cells were pulsed with 4-thiouridine for 2 hours and then RNA was extracted at 0, 2, 4, and 7 hr time-points in quadruplicate from each cell line. 4sU labeling followed by RNA-seq was then used to measure the abundance of transcripts in each population. A decay rate was estimated based on the rate at which transcript abundance was reduced at these time-points.

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Project description:We used RNA sequencing to compare MDA-MB-231 cells to their higly metastatic MDA-LM2 derivatvies.

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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.

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MDA-MB-231-LM2 cells treated with sudemycin D6 (SD6)

Project description:MDA-MB-231-LM2 cells treated with sudemycin D6 (SD6)

| PRJNA686063 | ENA

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.

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

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Intact extracellular vesicle cross-linking on vesicles derived from MDA-MB-231 and LM2 cells

Project description:The development of any pharmaceutical requires characterization of the compound, usually be several techniques. Therefore, characterizing the protein content and biochemical state of EVs is of great importance for their useif they are to be used as biopharmaceuticals. Structural characterization of proteins in EVs remains a great challenge even for state-of-the-art technologies such as super-resolution and electron microscopy, partly due to the biophysical and biochemical heterogeneity of EVs. Here we overcome some of these challenges by using cross-linking mass spectrometry (XL-MS) to structurally characterize protein complexes and the interactome of intact EVs, at an unprecedented resolution of up to 30Å. By applying XL-MS to intact EVs derived from two metastatic breast cancer cell lines (MDA-MB-231 and LM2), we validate the presence of active forms of protein complexes that are known to play a role metastasis, revealing for example previously uncharacterized regions of Moesin. Moreover, a cross-linking data-driven molecular docking supports novel conformations of ANXA2 in LM2 EVs.

2022-11-08 | PXD029591 | Pride

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