Transformation mechanism of human choriocarcinoma

本研究旨在探讨绒毛膜癌变的发生机制。鉴定绒毛膜癌变的致癌基因对这一目的非常重要。采用NIH3T3和4CY-4-3细胞进行DNA转染。后者是由腺病毒4型诱导的不完全转化细胞。然而，二次转染后从疫源地获得的DNA丢失了Alu重复序列。因此，我们在5种绒毛膜癌细胞中进行了Southern和Northern印迹实验，以研究已知的癌基因的重排和表达状况。11-13种癌基因在这些细胞中不同程度地表达，但在一个细胞中观察到c-myc癌基因重排。由于本部分未提及这些不同癌基因的表达，因此认为滋养细胞基因组的不稳定性在恶性转化中起重要作用。在单精子、雄激素性痣细胞中观察到丝裂霉素C的存在和染色体畸变对SCE的高诱导，支持了这一假设。

The Present research project was undertaken to explore the mechanism of choriocarcinogenesis. Identification of the oncogene responsible for choriocarcinogenesis was important for this purpose. DNA transfection was performed by the use of NIH3T3 and 4CY-4-3 cell. The latter was incompletely transformed cell induced by adenovirus type4. However, DNA obtained from the foci following the secondary transfection lost the Alu repeat. Thus, Southern and Northern blots were tried in 5 kinds of choriocarcinoma cells in order to investigate rearrangements and expression status of the already-known orcogenes. 11-13 kinds of oncogenes were expressed in various degrees in these cells although rearrangement of c-myc oncogene was observed in one cell. Since expression of such various oncogenes has not been referred in the part, genomic instability in trophoblast was assumed to play an important role for the malignant transformation. A high induction of SCE with the presence of mitomycin C and chromosome aberrations with its absence observed in cells from monospermic, androgenetic mole would support this assumption.