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Lipid remodeling in response to methionine stress in MDA-MBA-468 triple-negative breast cancer cells

ABSTRACT: Lipid remodeling in response to methionine stress in MDA-MBA-468 triple-negative breast cancer cells

PROVIDER: PRJNA656377 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12419529.fastq.gz	Fastqsanger.gz
	SRR12419530.fastq.gz	Fastqsanger.gz
	SRR12419531.fastq.gz	Fastqsanger.gz
	SRR12419532.fastq.gz	Fastqsanger.gz
	SRR12419533.fastq.gz	Fastqsanger.gz

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Lipid remodeling in response to methionine stress in MDA-MBA-468 triple-negative breast cancer cells

Project description:Methionine is an essential amino acid and critical precursor to the cellular methyl donor S-adenosylmethionine. Unlike non-transformed cells, cancer cells have a unique metabolic requirement for methionine and are unable to proliferate in growth media where methionine is replaced with its metabolic precursor, homocysteine. This metabolic vulnerability is common among cancer cells regardless of tissue origin and is known as “methionine dependence”, “methionine stress sensitivity”, or Hoffman effect. Here, we characterize the response of lipids to methionine stress in the triple negative breast cancer cell line MDA-MB-468 and its methionine stress insensitive derivative, MDA-MB-468res-R8. Lipidome analysis identified an immediate, global decrease in lipid abundances with the exception of triglycerides and an increase in lipid droplets in response to methionine stress specifically in MDA-MB468 cells. Furthermore, specific gene expression changes were observed as a secondary response to methionine stress in MDA-MB-468, resulting in a down-regulation of fatty acid metabolic genes and up-regulation of genes in the unfolded protein response pathway. We conclude that the extensive changes in lipid abundance during methionine stress is a direct consequence of the modified metabolic profile previously described in methionine stress sensitive cells. The changes in lipid abundance likely results in changes in membrane composition inducing the unfolded protein response we observe.

2020-08-11 | GSE155955 | GEO

Transcriptional heterogeneity of MDA-MBA-468 triple-negative breast cancer cells

Project description:Transcriptional heterogeneity of MDA-MBA-468 triple-negative breast cancer cells

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Transcriptional heterogeneity among MDA-MBA-468 triple-negative breast cancer cells

Project description:Transcriptional heterogeneity among MDA-MBA-468 triple-negative breast cancer cells

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Lipid remodeling in response to methionine stress in MDA-MBA-468 triple-negative breast cancer cells.

Project description:Methionine (Met) is an essential amino acid and critical precursor to the cellular methyl donor S-adenosylmethionine. Unlike nontransformed cells, cancer cells have a unique metabolic requirement for Met and are unable to proliferate in growth media where Met is replaced with its metabolic precursor, homocysteine. This metabolic vulnerability is common among cancer cells regardless of tissue origin and is known as "methionine dependence", "methionine stress sensitivity", or the Hoffman effect. The response of lipids to Met stress, however, is not well-understood. Using mass spectroscopy, label-free vibrational microscopy, and next-generation sequencing, we characterize the response of lipids to Met stress in the triple-negative breast cancer cell line MDA-MB-468 and its Met stress insensitive derivative, MDA-MB-468res-R8. Lipidome analysis identified an immediate, global decrease in lipid abundances with the exception of triglycerides and an increase in lipid droplets in response to Met stress specifically in MDA-MB-468 cells. Furthermore, specific gene expression changes were observed as a secondary response to Met stress in MDA-MB-468, resulting in a downregulation of fatty acid metabolic genes and an upregulation of genes in the unfolded protein response pathway. We conclude that the extensive changes in lipid abundance during Met stress is a direct consequence of the modified metabolic profile previously described in Met stress-sensitive cells. The changes in lipid abundance likely results in changes in membrane composition inducing the unfolded protein response we observe.

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Transcriptional heterogeneity among subclonal populations of MDA-MBA-468 triple-negative breast cancer cells

Project description:Transcriptional heterogeneity among subclonal populations of MDA-MBA-468 triple-negative breast cancer cells

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Transcriptional heterogeneity among xenograft tumors derived from subclonal populations of MDA-MBA-468 triple-negative breast cancer cells

Project description:Transcriptional heterogeneity among xenograft tumors derived from subclonal populations of MDA-MBA-468 triple-negative breast cancer cells

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RNA-Sequencing of MDA-MB-468 TNBC cells, carboplatin-resistant isogenic MDA-MB-468 cells, and dN90-beta-catenin-overexpressing MDA-MB-468 cells

Project description:In this experiment, we generated isogenic carboplatin-resistant MDA-MB-468 cells displaying a 5x increase in IC50 in respect to the parental cell line. We set out to compare the transcriptome of these cell lines, together with MDA-MB-468 cells overexpressing a constitutively active form of beta-catenin to understand underlying transcriptional changes supporting stable carboplatin-tolerance.

2021-07-09 | E-MTAB-10337 | biostudies-arrayexpress

Transcriptomic differences between radioresistant MDA-MB-468 and parental MDA-MB-468

Project description:Transcriptomic differences between radioresistant MDA-MB-468 and parental MDA-MB-468

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RNA-seq analysis of triple negative breast cancer cell line MDA-MB-468 with knockdown of cytokeratin 5 (CK5)

Project description:MDA-MB-468 cells expressing pLK0-shControl or pLK0-shCK5-425222

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ALDH1A3-mediated gene expression in MDA-MB-231 cells and MDA-MB-468 cells

Project description:To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells

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