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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43895 | GEO | 2013/06/30

SECONDARY ACCESSION(S): PRJNA188078

REPOSITORIES: GEO

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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.

2013-06-30 | E-GEOD-43895 | biostudies-arrayexpress

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

| 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. 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 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

Lysine producing mutant K051

Project description:Isolation of a new lysine producing C. glutamicum mutant

| PRJEB21 | ENA

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

Proteome of Control versus shKDM2B in MDA-MB-231 Cells

Project description:Project comparing the proteome between control and knockdown of KDM2B in MDA-MB-231 cell lines. Previous data demonstrated that knockdown of KDM2B induced transcriptional changes in ribosomal and metabolic gene targets and thus TMT proteomics was pursued to compare the protein level changes that occur after knockdown of KDM2B.

2023-11-22 | PXD046970 | Pride

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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