Dataset: shRNAi profiling of human MDA-MB-231 cells expressing anti-p53 (shp53) short-hairpin RNAs treated with TFGbeta or control

TGFβ ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. We now show that TGFβ-dependent cell migration, invasion and metastasis are empowered by mutant-p53. To investigate the specific gene expression program by which mutant-p53 and TGFβ control invasion and metastasis in breast cancer cells, we compared the TGFβ transcriptomic profile of control and mutant-p53 depleted MDA-MB-231 cells. Experiment Overall Design: MDA-MB-231 cells, stably expressing either control (shGFP) or anti-p53 (shp53) short-hairpin RNAs, were left untreated or treated with TGFbeta. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the 4 conditions (1: untreated control; 2: TGFbeta treated control; 3: untreated p53-depleted cells; 4: TGFbeta treated mutant-p53-depleted cells), for a total of 16 samples.

Species:

human

Samples:

16

Source:

E-GEOD-14491

PubMed:

19345189

Updated:

Dec.12, 2014

Registered:

Sep.11, 2014