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

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

PROVIDER: PRJNA765010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15997900_1.fastq.gz	Fastqsanger.gz
	SRR15997900_2.fastq.gz	Fastqsanger.gz
	SRR15998000_1.fastq.gz	Fastqsanger.gz
	SRR15998000_2.fastq.gz	Fastqsanger.gz
	SRR15997901_1.fastq.gz	Fastqsanger.gz

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

Project description:Intratumoral heterogeneity has been described for various tumor types and models of human cancer, and can have profound effects on tumor progression and drug resistance. This study describes transcriptional heterogeneity among subclonal populations (SCPs) derived from a single triple-negative breast cancer cell line.

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Transcriptional heterogeneity among xenograft tumors derived from subclonal populations of 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 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.

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

Project description:Lipid remodeling in response to methionine stress in 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.

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