Antisense RNA to the type I insulin-like growth factor receptor reversed the transformed phenotype of PC-3 human prostate cancer cell line in vitro

The insulin-like growth factor I receptor [IGF-IR] plays an essential role in the establishment and maintenance of transformed phenotype. Interference with the IGF- IR pathway by antisense causes reversal of the transformed phenotype in many rodent and human tumor cell lines. We stably transfected the PC-3 human prostate cancer cell line with an IGF-IR antisense RNA expression plasmid. The number of lGF-I receptors on the antisense-transfected PC-3 cells was reduced by 40.2% relative to the control-transfected cells. The transfected cells maintained their high expression of IGF-IR antisense RNA for up to one year in selective medium. The reduction in the expression of IGF-IR had no effect on the cell growth in monolayer. The clonogenicity of antisense-transfected cells was 24.7% of the clonogenicity of control-transfected cells in soft agar. There was a good correlation between IGF-IR level and inhibition of transformation in soft agar. These results indicate that reduction of IGF-IR by antisense RNA can reverse the transformed phenotype of human prostate cancer cells

[Genetics of testicular germ cell tumors]

Testicular germ cell tumor [TGCT] is the most solid tumor in 20 - 40 years old man. TGCT account for 95% of testicular tumors and represent a unique type of human cancer from several different perspectives. TGCT arise by transformation of germ cells. The Transformed germ cells exhibit ploripotentially to differentiate into embryonic. Extra-embryonic, and somatic tissue types, and are highly sensitive to cisplatin-based chemotherapy. Investigation into the genetics of TGCT can provide methods of molecular diagnosis and help to the understanding of molecular basis of transformation, differentiation and sensitivity/resistance. The molecular basis for the chemosensitivity of these tumors is poorly understood, although initial studies suggest that wild-type p53 might play a central role, further studies will provide insights into why other solid tumors remain far from curable. The following review will provide information about genetic altration and chromosomal aberration occur in TGCT. These studies have identified multiplication of 12p, manifested in I [12p] or tandem duplication of 12p. As a unique change in TGCT which serves as a diagnostic marker. These data also indicate that multiple genetic events play a role in distinct pathways in the development of TGCT, and further elucidation of the underlying genetic and biochemical mechanisms is central to unraveling biology and improving treatment of TGCT