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p53 Enters the MicroRNA World
Heiko Hermeking1,
1 Molecular Oncology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany
Corresponding author
Heiko Hermeking
Recently, microRNAs, which are regulated by the transcription factor encoded by the tumor suppressor gene p53, were identified independently by seven groups. Their studies highlight the microRNAs miR-34a and miR-34b/c as direct, conserved p53 target genes that presumably mediate induction of apoptosis, cell cycle arrest, and senescence by p53. Since these microRNAs may regulate the levels of hundreds of different proteins, these findings add a new, challenging layer of complexity to the p53 network. The initial evidence suggesting that miR-34 genes are central mediators of p53 function is summarized here.
附：
Molecular Oncology (Heiko Hermeking, MPG)
The aim of our group is to understand the function and regulation of the transcription factors p53 and c-MYC, as well as the processes and genes which they regulate. c-MYC and p53 are encoded by genes which are altered in more than 50% of all cancers. The tumor suppressor gene product p53 is activated after DNA damage and induces genes, as 14-3-3sigma, which mediate cell cycle inhibition. We are studying the biology of 14-3-3sigma by structural, proteomic and genetic approaches. p53 is an integral part of a program that mediates cellular senescence and preserves genomic integrity. In contrast, activation of the c-MYC oncogene leads to immortalization and genomic instability. How these effects of oncogenic c-MYC activation are mediated is a focus of our studies. In addition, we are identifying and characterizing genetic and epigenetic alterations which contribute to prostate cancer and malignant melanoma.
