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Series GSE109373 Query DataSets for GSE109373
Status Public on Jan 19, 2018
Title Mutant p53 controls tumor metabolism and metastasis by regulating PGC-1α
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Mutant forms of p53 protein often possess pro-tumorigenic function, conferring increased survival and migration to tumor cells via its “gain of function” activity. Whether and how a common polymorphism in TP53 at amino acid 72 (Pro72Arg, hereafter P72 and R72) impacts this gain of function has not been determined. We show that mutant p53 enhances migration and metastasis of tumors through the ability to bind and regulate PGC-1α, and that this regulation is markedly impacted by the codon 72 polymorphism. Tumor cells with the R72 variant of mutant p53 show increased PGC-1α function, along with greatly increased mitochondrial function and metastatic capability. Breast cancers containing mutant p53 and the R72 variant show poorer prognosis compared to P72. The combined results reveal PGC-1α as a novel “gain of function” partner of mutant p53, and indicate that the codon 72 polymorphism influences the impact of mutant p53 on metabolism and metastasis.
Overall design RNA-seq analysis of R175H and R273H mutant, P72- and R72-polymorphism H1299 cells
Contributor(s) Murphy M, Basu S
Citation(s) 29463573
Submission date Jan 18, 2018
Last update date Mar 26, 2019
Contact name Priyankara J Wickramasinghe
Phone 2154956837
Organization name The Wistar Institute
Department Bioinformatics
Lab Genomics
Street address 3601 Spruce Street
City Philadelphia
State/province PA
ZIP/Postal code 19104
Country USA
Platforms (1)
GPL18573 Illumina NextSeq 500 (Homo sapiens)
Samples (11)
GSM2940626 H1299.175P.1
GSM2940627 H1299.175P.2
GSM2940628 H1299.175P.4
BioProject PRJNA430702
SRA SRP131048

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Supplementary file Size Download File type/resource
GSE109373_H1299_RNAseq.txt.gz 1.9 Mb (ftp)(http) TXT
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Raw data are available in SRA
Processed data are available on Series record

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