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Gene expression profiling of mouse mammary tumorspheres, mammospheres, and mammospheres induced to differentiate

ABSTRACT: Tumorpsheres and mammospheres were used to propagate mouse breast tumor-initiating cells and their normal stem/progenitor counterparts, respectively. Mammospheres induced to differentiate were used to model the more differentiated cells of the mouse mammary gland. We used microarrays to find differentrially expressed genes between tumorspheres, mammospheres, and mammospheres induced to differentiate

ORGANISM(S): Mus musculus

PROVIDER: GSE32463 | GEO | 2012/01/30

SECONDARY ACCESSION(S): PRJNA147875

REPOSITORIES: GEO

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Project description:Purpose: The goals of this study is to compare and examine the transcriptional profile in the secondary mammospheres of control versus CIC-deficient T47D cells by mRNA sequencing and to understand the molecular basis of the CIC regulation of CSC-like properties in luminal type of breast cancer cells. Methods: DNA library for mRNA sequencing of secondary mammospheres derived from control and CIC-deficient T47D breast cancer cells was prepared using a TruSeq Stranded Total RNA LT Sample Prep Kit (Gold) and their libraries sequenced on the NovaSeq sequencer accompanying the NovaSeq 6000 S4 Reagent Kit. The trimmed reads that passed quality filters were mapped to reference genome with HISAT2, followed by assembly of transcript with StringTie. Results: A total of 20377 genes were differentially expressed (10438 upregulated and 9939 downregulated) in the CIC-deficient T47D mammospheres when compared with control mammospheres. Approximately 5% of the transcripts showed differential expression between the control and CIC-deficient secondary mammospheres, with a fold change ≥1.2 and p value <0.05. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses revealed that CIC-deficient mammospheres differentially expressed genes that are involved in processes associated with cancer progression such as cell cycle, cell proliferation, cell growth, and apoptotic process, as well as autoimmunity. Conclusions: Our results show the first comparative analysis of secondary mammospheres derived from control and CIC-deficient T47D breast cancer cells. The data reported here should also provide reference for expression profiles of CSC-like cells in ER+/PR+/HER2- luminal breast cancer cells. We conclude that CIC deficiency promotes CSC-like properties and thus breast cancer progression through controlling CSC-related pathways including focal adhesion and extracellular matrix (ECM)-receptor interactions, and may also regulate cell cycle, cell proliferation, and apoptosis.

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Gene expression profiling of mouse mammary tumorspheres, mammospheres, and mammospheres induced to differentiate

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