Identification of Pro-Differentiation p53 Target Genes and Evaluation of Expression in Normal and Malignant Mammary Gland
Abstract
Ectopic delta-N-p63 could block retinoic acid induced differentiation in embryonic carcinoma cells NT2/D1, and preserve transcript level of nestin post RA treatment. Similarly, RA treatment could inhibit the proliferation of breast cancer cell lines, and down-regulate the mRNA level of some self-renew relative genes including oct3/4, nanog and dab2 in these cells. Immunocytoflurescence staining detected existence of delta-N-p63 in both estrogen receptor negative cells such as SUM102, SUM149 and MDA-MB-231 cells, but also MCF-7 cells with luminal epithelial phenotype. And delta-N-p63 positive cells are not well-differentiated and lost expression of cell cycle marker ki-67, cyclin D1. Infection of breast cancer cells with delta-N-p63 adeovirus could decrease cell growth rate, cause G1/G0 cell phase arrest. In MCF-7 cell, ectopic delta-N-p63 could induce cells to lost expression of ki- 67 and cyclin D1. Semi-quantitative PCR assay showed that over expression of delta-N-p63 had diverse effect on transcript level of some self-renew correlating gene events such as TA-P63, oct3/4, nanog, sonic hedgehog, hTERT, ect.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2007
- Accession Number
- ADA471561
Entities
People
- Hua Li
Organizations
- Geisel School of Medicine