Transcriptome analysis of QPRT silencing in breast cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE151521 | GEO | 2020/06/01
REPOSITORIES: GEO
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Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101). Two-condition experiment, MCF10A-vector control vs. MCF10A-TRIM29 shRNA cells; MCF7-vector control vs. MCF7-TRIM29 cells.
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Project description:Tartrate-resistant acid phosphatase (TRAP/ACP5) is a metalloenzyme of the group of acid phosphatases. High levels of TRAP protein have been associated with the development of cancer metastasis and with clinically relevant parameters of cancer progression and cancer aggressiveness. In order to investigate the molecular pathways responsible for the role of TRAP in such cancer related processes, we examined the changes in the proteome and phosphoproteome of MDA-MB-231 breast cancer cells determined by TRAP protein overexpression or knock-down. The dataset contains two different experimental setups. The first setup consists of the comparison between MDA-MB-231 breast cancer cells stably transfected with a full-length rat TRAP (TRAP3high) and MDA-MB-231 cells transfected with a mock insert (ctrl). The second setup consists of the comparison between TRAP3high cells transfected with a scrambled shRNA (scr) and TRAP3high cells transfected with either of two shRNAs targeting TRAP (sh2 and sh3+4). In the first experimental setup, we performed quantitative phosphoproteomic and proteomic analyses using SILAC. The two analyses identified respectively 3,290 unique phosphorylation sites corresponding to 1,059 genes, and 7,957 proteins corresponding to 7,846 genes. In the second experimental setup, we performed quantitative proteomics analysis using TMT, identifying 9,848 proteins corresponding to 9,189 genes. Integrated analysis of the generated data revealed a regulation of proteins involved in the cell adhesion process and extracellular matrix organization network. In particular, TGFβ isoform 2 (TGFβ2), TGFβ receptor type 1 (TβR1) and SMAD2 protein levels were increased upon TRAP upregulation, as well as phosphorylation of CD44 on residues localized in the intracellular portion of the protein. Finally, these results were validated by functional blocking and chemical inhibition of TGFβ2/TβR, which decreased TRAP-dependent cell migration and proliferation, and by blocking of CD44, which reduced TRAP3high cell proliferation. Altogether, we show that TRAP promotes metastasis-related cell properties in breast cancer cells via TGFβ2/TβR and CD44, thereby identifying a potential signaling mechanism associated to TRAP action in breast cancer cells.
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