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Expression analysis of MDA-MD-231 cells that express lysine racemase (lyr) when grown on D-Lysine versus L-Lysine

ABSTRACT: This experiment aimed to investigate whether cells that express the L-Lysine-producing enzyme lyr exhibit any mRNA changes when grown on precursor D-Lysine relative to L-Lysine. Total RNA obtained from lyr-expressing MDA-MB-231 cells after 3 days in culture with amino acid precursor D-Lysine, L-Lysine, or starved of both.

ORGANISM(S): Homo sapiens

SUBMITTER: Nicholas Gauthier

PROVIDER: E-GEOD-43895 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression analysis of MDA-MD-231 cells that express lysine racemase (lyr) when grown on D-Lysine versus L-Lysine

2013-06-30 | GSE43895 | GEO

Expression analysis of 3T3 cells that express Arabidopsis-derived Diaminopimelate Decarboxylase (DDC) in response to growth on meso-2,6-diaminopimelic acid (DAP) versus L-Lysine

Project description:This experiment aimed to investigate whether cells that express the L-Lysine-producing enzyme DDC exhibit any mRNA changes when grown on precursor DAP relative to L-Lysine. Total RNA obtained from DDC-expressing 3T3 cells after 3 days in culture with amino acid precursor DAP, L-Lysine, or starved of both.

2013-06-30 | E-GEOD-43894 | biostudies-arrayexpress

Expression analysis of MDA-MD-231 cells that express lysine racemase (lyr) when grown on D-Lysine versus L-Lysine

Project description:This experiment aimed to investigate whether cells that express the L-Lysine-producing enzyme lyr exhibit any mRNA changes when grown on precursor D-Lysine relative to L-Lysine. Total RNA obtained from lyr-expressing MDA-MB-231 cells after 3 days in culture with amino acid precursor D-Lysine, L-Lysine, or starved of both.

| S-ECPF-GEOD-43895 | biostudies-other

Expression analysis of 3T3 cells that express Arabidopsis-derived Diaminopimelate Decarboxylase (DDC) in response to growth on meso-2,6-diaminopimelic acid (DAP) versus L-Lysine

Project description:This experiment aimed to investigate whether cells that express the L-Lysine-producing enzyme DDC exhibit any mRNA changes when grown on precursor DAP relative to L-Lysine.

2013-06-30 | GSE43894 | GEO

MiRNA 3613-5p and MiRNA 3916 rescued the inhibition of cell migration in CNOT2 depleted MDA-MD-231 cells.

Project description:BackgroundThe CCR4-NOT complex (CNOT) plays an important role in regulating translation repression. Here, silencing of the complex via the transfection of MDA-MB-231 breast cancer cells with CNOT2 Small interfering RNA (siRNA) decreased the mRNA expression of DiGeorge Syndrome Critical Region 8 (DGCR8) and Dicer.MethodsGene expression profiling using an miRNA array was carried out with CNOT2 siRNA treated MDA-MB-231 cells. After transfection with CNOT2 siRNA, qRT-PCR was used to see the level of Dicer and DGCR8. PANTHER pathway analysis was used to see the biological function of microRNAs (miRNAs or miRs).ResultsCNOT2 siRNAs were attenuated the mRNA levels of Dicer and DGCR8. An analysis of miRNAs in CNOT2 silenced MDA-MB-231 cells using miRNA array revealed that 42 miRNAs, including has-miR-7, has-miR-4283, has-miR-10a were significantly upregulated while 47 miRNAs, including has-miR-3916 and has-miR-3613-5p were downregulated following CNOT2 silencing in MDA-MB-231 cells. Also, has-miR-3613-5p and has-miR-3916 rescued the inhibition of migration from CNOT2 short hairpin RNA (shRNA) MDA-MB-231 stable cell lines. PANTHER pathway analysis assigned the miRNAs to multiple processes, including Wnt signaling, angiogenesis, cadherin signaling, inflammation mediated by chemokine and cytokine signaling, integrin signaling, EGF receptor signaling and Huntington's disease.ConclusionsTogether, our findings provide useful target genes for understanding the molecular mechanisms of CNOT2 in breast cancer.

| S-EPMC8799183 | biostudies-literature

Transcriptomic profiling of MDA-MD-231 and MDA-MB-231-LM1 cells isolated from mouse lungs at micrometastatic stage

Project description:Cancer-associated fibroblasts promote the development of many primary malignancies, but their function in metastatic progression is poorly understood. Here, we demonstrate that colonization of the lungs by metastatic breast cancer cells induces an inflammatory phenotype in lung fibroblasts. CXCL9 and CXCL10 are induced in an NFκB-dependent manner in metastasis-associated fibroblasts in response IL-1α and IL-1β secreted by disseminated breast cancer cells. We find that the chemokine receptor CXCR3, that binds CXCL9/10, is expressed in a small subset of breast cancer cells that exhibits greater tumor-initiating ability when co-transplanted with fibroblasts. CXCR3-expressing cancer cells maintain JNK signaling that drives IL-1A/B expression, and thus rendering this subpopulation efficient in both inducing CXCL9/10 in lung fibroblasts and responding to the chemokines. Importantly, disruption of the CXCL9/10-CXCR3 axis significantly reduces metastatic colonization in xenograft and syngeneic mouse models suggesting an essential role of this paracrine crosstalk in metastatic progression and a potential therapeutic vulnerability for the treatment of metastatic breast cancer.

2020-02-17 | GSE121944 | GEO

MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5

Project description:Elf5 induced transcriptional changes in MDA-MB-231 origin, control (mut Elf5) vs WT ELF5 Two-condition experiment, control (mut-Elf5) vs WT-Elf5. Each has 3 biological repeats.

| S-ECPF-GEOD-32144 | biostudies-other

miRNA expression profile in MDA-MB-231 cells on LPA stimulation

Project description:LPA is a natural bioactive lipid with growth factor-like functions due to activation of series of six G protein-coupled receptors (LPA1-6). In this study we determine the LPA induced early-miRNA expression profile in human breast cancer cell lines MDA-MB-231 MDA-MB-231 cells were serum starved for 24h and then stimulated with LPA (1µM) for 45min. The controls were the serum starved unstimulated cells. Three replicates were included in this study.

2015-05-05 | E-GEOD-64100 | biostudies-arrayexpress

Metabolic Regulation of Gene Expression by Histone Lysine Ã-hydroxybutyrylation [RNA-seq]

Project description:We identified a new type of histone mark-lysine Ã-hydroxybutyrylation (Kbhb). This ketone body derived histone mark (Kbhb) was dramatically induced in livers during starvation. To charactize histopne Kbhb: 1) We mapped genomic distributions of histone Kbhb marks (H3K9bhb, H3K4bhb and H4K8bhb) by ChIP-seq in mouse liver. 2) We examined the response of histone Kbhb mark to starvation by carrying out ChIP-seq experiments for H3K9bhb in both "starved" and "fed" mouse liver. 3) We also examined differentially-expressed genes during starvation by carrying out RNA-seq experiments in both "starved" and "fed" mouse liver. By integrating analyses of ChIP-seq and RNA-seq data, we tried to get a correlation between H3K9bhb mark and gene expression in response to starvation. Sequencing was performed on the HiSeq2000 (Illumina). RNA-seq of mouse liver cells both in "starved" and "fed" conditions.

2016-04-06 | E-GEOD-69616 | biostudies-arrayexpress

Effects of FSTL1 on cell proliferation in breast cancer cell line MDA‑MB‑231 and its brain metastatic variant MDA‑MB‑231‑BR.

Project description:In the past decades, altered Follistatin‑like 1 (FSTL1) expression has been documented in a variety of cancers, while its functional roles are poorly understood. Particularly in breast cancer, the expression of FSTL1 and its signaling pathway remain to be determined. In the present study, an elevated FSTL1 expression and a supressed cell proliferation were detected in a specific brain metastatic cell line MDA‑MB‑231‑BR (231‑BR), compared with its parental cell line MDA‑MB‑231. However, this protein was hardly detected in the other three breast cancer cell lines. Next, lentiviral vectors encoding FSTL1 or FSTL1 specific shRNAs were used to overexpress or knock down FSTL1 in MDA‑MB‑231 or 231‑BR, respectively (MDA‑MB‑231FSTL1 or 231‑BRsh FSTL1). Results showed that overexpression of FSTL1 inhibited MDA‑MB‑231 cell proliferation, while knockdown of FSTL1 in 231‑BR cells promotes cell proliferation, compared with their corresponding control groups. These results were further confirmed in nude mouse xenografts. The tumor volume in 231‑BR cell-bearing mice was significantly smaller than that of MDA‑MB‑231 group, and reduction of tumor volume was detected in MDA‑MB‑231FSTL1 cell-bearing mice compared with the control group. Previous studies revealed that TGF‑β-Smad2/3 signaling pathway was activated in 231‑BR and MDA‑MB‑231FSTL1 cells, which may contribute to the inhibited cell proliferation. In addition, Smad3 knockdown could restore the inhibition of cell proliferation induced by FSTL1 overexpression in MDA‑MB‑231FSTL1 cells, indicating that the anti‑proliferative effect of FSTL1 overexpression may be associated with Smad3 involved TGF‑β signaling pathway regulation. This study identified FSTL1 as an inhibitor of cell proliferation in MDA‑MB‑231 and 231‑BR cell lines, which may provide new insights into the development and management of breast cancer.

| S-EPMC5780039 | biostudies-literature

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