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    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; CELL ; Germany ; INHIBITION ; THERAPY ; PROTEIN ; BINDING ; papillomavirus ; FORM ; IDENTIFICATION ; genetics ; cervical cancer ; CERVICAL-CANCER ; p53 ; human papillomavirus ; CERVICAL-CARCINOMA CELLS ; E6 ; DEGRADATION ; POSITIVE CANCER-CELLS ; AFFINITY ; VARIANT ; THERAPIES ; cancer therapy ; LIBRARIES ; TYPE-16 E6 ; development ; P53 ACTIVITY ; oncogenes ; E6-AP
    Abstract: Specific types of human papillomaviruses (HPVs) cause cervical cancer. The viral E6 oncogene is a critical factor for maintaining the malignant phenotype of HPV-positive tumour cells. By yeast two-hybrid screening of a randomised peptide expression library, we isolated linear short peptides, which specifically bind to the HPV16 E6 oncoprotein. Sequence alignments and mutational analyses of the peptides identified a hitherto undiscovered E6-binding motif. Intracellular expression of a peptide containing the novel E6-binding motif resulted in inhibition of colony formation capacity, specifically of HPV16-positive cancer cells. A solubility-optimised variant of the peptide was created, which binds to HPV16 E6 with high affinity. Its intracellular expression efficiently induced apoptosis in HPV16-positive cancer cells. This was linked to restoration of intracellular p53 activities. Thus, this newly identified E6-binding motif could form a novel basis for the development of rational strategies for the treatment of HPV16-positive preneoplastic and neoplastic lesions
    Type of Publication: Journal article published
    PubMed ID: 19099279
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