02 Dec 2022
30 Nov 2022
Human papillomavirus type 16 (HPV 16) is involved in the infection and transformation of malignant cells leading to the development of cervical cancer in 70% of cases. The HPV 16 genome encodes six early proteins including the HPV 16 E6 oncoprotein, which deregulate cell proliferation by interfering tumor suppressor p53.As well, HPV 18 E7 oncoprotein dysregulate pRb. Consequently, the cell cycle is disrupted inducing DNA damage, genomic instabilities as well as structural or numerical chromosomal aberrations. This study aimed to explore the karyotype of rat myoblast murine L6-transfected cells with HPV 16 in order to identify any chromosomal aberrations. Karyotype analysis was performed by standard G banding technique of HPV 16 L6 transfected rat myoblast cells and control L6 rat myoblast cells. Electroporation was used for the HPV 16 DNA exogenous transfection of rat myoblast cell L6. The chromosomal map reveals chromosomal aberrations illustrated in the translocation ideogram. The results shown that in approximately 80% of the cells there is a copy of a chromosome resulting from a Robertsonian translocation between the long arm of two chromosomes and 50% of the cells show double minutes. Our findings indicate a highly significant link between HPV 16 and chromosomal aberrations of infected cells. That suggests a very likely link between these and cervical cancer. Further studies on human cell samples are needed to provide better evidence for this binding.