Quantitative TP73 Transcript Analysis in Hepatocellular Carcinomas

摘要: Purpose: The p53 family member p73 displays significant homology to p53, but data from primary tumors demonstrating increased expression levels of in the absence any gene mutations argue against a classical tumor suppressor function. A detailed analysis protein tissues has revealed two classes isoforms. Whereas proapoptotic, full-length, transactivation-competent (TA-p73) putative activity similar antiapoptotic, NH2-terminally truncated, transactivation-deficient been shown possess oncogenic activity. proteins can be generated by following different mechanisms: (a) aberrant splicing (p73ex2, p73ex2/3, N-p73) and (b) alternative promoter usage second intronic (N-p73). purpose our study was elucidate origin TA-p73 isoforms hepatocellular carcinomas. Experimental Design: We analyzed underlying mechanisms overexpression cancer cells quantification transcripts 10 carcinoma patients using isoform-specific real-time reverse transcription-PCR. Results: Our demonstrate that only aberrantly spliced TA show significantly whereas N-p73 transcript is not up-regulated. Conclusions: Although we patient samples results strongly suggest elevated first (TA promoter) accounts for high-level both full-length tissues.