RNA sequencing data from MCF10AT cells expressing hPRLrL/hPRLrI or hPRLrL/hPRLrI I-tail removal mutant

The intermediate hPRLr (hPRLrI) is produced by alternative splicing which induces a frameshift, resulting in a novel 13 amino acid tail ("I-Tail") gain and a premature stop codon. hPRLrI induces significant proliferation and anchorage-independent growth of normal mammary epithelia when co-expressed with long form hPRLr (hPRLrL). hPRLrL and hPRLrI co-expression are necessary to induce the transformation of mammary epithelia. In studying the function of hPRLrI I-tail, the ubiquitin-like protein neural precursor cell expressed developmentally down-regulated protein 8 (NEDD8) was found to be interacting with the I-tail by yeast two-hybrid analysis. hPRLrI I-tail deletion results in attenuated ERK1/2 signaling, decreased anchorage-independent growth, and decreased cell motility. The goal of this study was to generate mRNA profiles for MCF10AT cells expressing hPRLrL/hPRLrI, or hPRLrL/hPRLrI I-tail removal mutant treated with or without prolactin (PRL). Overall design: To examine role of hPRLrI I-tail in the pathogenesis of breast cancer, mRNA profiling of MCF10AT cells expressing either hPRLrL/hPRLrI, or hPRLrL/hPRLrI I-tail removal mutant treated with or without prolactin (PRL) for 2 hours.