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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells

ABSTRACT: Comparison of gene expression between the breast cancer cell line MDA-MB-231 and its highly metastatic deriviate LM2 cells (described in Minn et al., Nature 2005). Results hilghlights potential metastasis promoting and suppressing genes. 4 Samples

ORGANISM(S): Homo sapiens

SUBMITTER: Png KJ

PROVIDER: S-ECPF-GEOD-23904 | biostudies-other | 2012 Jan

REPOSITORIES: biostudies-other

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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells.

Project description:Comparison of gene expression between the breast cancer cell line MDA-MB-231 and its highly metastatic deriviate LM2 cells (described in Minn et al., Nature 2005). Results hilghlights potential metastasis promoting and suppressing genes.

2011-12-16 | GSE23904 | GEO

Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells.

2011-12-16 | E-GEOD-23904 | biostudies-arrayexpress

miR-126 over-expression in highly metastatic LM2 breast cancer cells

Project description:miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells. 4 Samples

| S-ECPF-GEOD-23905 | biostudies-other

miR-126 over-expression in highly metastatic LM2 breast cancer cells.

2011-12-16 | GSE23905 | GEO

miR-126 over-expression in highly metastatic LM2 breast cancer cells.

2011-12-16 | E-GEOD-23905 | biostudies-arrayexpress

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

Comparing alternative polyadenylation landscapes in highly and poorly metastatic breast cancer cells

Project description:Cancer cells often co-opt post-transcriptional regulatory mechanisms to achieve pathologic expression of gene networks that drive metastasis. Translational control is a major regulatory hub in oncogenesis, however its effects on cancer progression remain poorly understood. To address this, we used ribosome profiling to compare genome-wide translation efficiencies of poorly and highly metastatic breast cancer cells and patient-derived xenografts. We developed novel regression-based methods to analyze ribosome profiling and alternative polyadenylation data, and identified HNRNPC as a translational controller of a specific mRNA regulon. Mechanistically, HNRNPC, in concert with PABPC4, binds near to poly(A) signals, thereby governing the alternative polyadenylation of a set of mRNAs. We found that HNRNPC and PABPC4 are downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs to undergo 3’ UTR lengthening and subsequently, translational repression. We showed that modulating HNRNPC expression impacts the metastatic capacity of breast cancer cells in xenograft mouse models. We also found that a small molecule, previously shown to induce a distal-to-proximal poly(A) site switching, counteracts the HNRNPC-PABPC4 driven deregulation of alternative polyadenylation and decreases the metastatic lung colonization by breast cancer cells in vivo.

2023-02-20 | GSE186637 | GEO

Fluvastatin-induced differential global gene expression in human metastatic MDA-MB-231 breast cancer cells

Project description:The current study analyzed the altered expression profiles of genes that are responsible for fluvastatin-induced breast cancer cell death in MDA-MB-231 cells (ER-ve basal breast cancer cells). Some of these altered gene expressions were further inter connceted to various pathways which may eventually be recognised as drug targets/ biomarkers in statin-sensitve breast cancer patients. To understand the differential gene expression profile in fluvastatin treated (24 h) malignant breast cancer cells with untreated malignant breast cancer cells.

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RNA sequencing of MDA-LM2 and MDA-Parental cells

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

2021-03-30 | GSE160953 | GEO

Serum-derived exosomes from mice with highly metastatic breast cancer transfer increased metastatic capacity to a poorly metastatic tumor.

Project description:Altered interaction between CD200 and CD200R represents an example of "checkpoint blockade" disrupting an effective, tumor-directed, host response in murine breast cancer cells. In CD200R1KO mice, long-term cure of EMT6 breast cancer, including metastatic spread to lung and liver, was achieved in BALB/c mice. The reverse was observed with 4THM tumors, an aggressive, inflammatory breast cancer, with increased tumor metastasis in CD200R1KO. We explored possible explanations for this difference. We measured the frequency of circulating tumor cells (CTCs) in peripheral blood of tumor bearers, as well as lung/liver and draining lymph nodes. In some cases mice received infusions of exosomes from nontumor controls, or tumor bearers, with/without additional infusions of anticytokine antibodies. The measured frequency of circulating tumor cells (CTCs) in peripheral blood was equivalent in the two models in WT and CD200R1KO mice. Increased metastasis in EMT6 tumor bearers was seen in vivo following adoptive transfer of serum, or serum-derived exosomes, from 4THM tumor bearers, an effect which was attenuated by anti-IL-6, and anti-IL-17, but not anti-TNFα, antibody. Anti-IL-6 also attenuated enhanced migration of EMT6 cells in vitro induced by 4THM serum or exosomes, or recombinant IL-6. Exosome cytokine proteomic profiles responses in 4THM and EMT6 tumor-bearing mice were regulated by CD200:CD200R interactions, with attenuation of both IL-6 and IL-17 in 4THM CD200(tg) mice, and enhanced levels in 4THM CD200R1KO mice. We suggest these cytokines act on the microenvironment at sites within the host, and/or directly on tumor cells themselves, to increase metastatic potential.

| S-EPMC4735763 | biostudies-other

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