Carbone M, Kajiwara E, Patch C T, Lewis A M, Levine A S, Dixon K
Viral Pathogenesis Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Cancer Res. 1989 Dec 1;49(23):6809-12.
Hamster cells, transformed in vitro by SV40, have been reported to secrete an unidentified factor(s) that inhibits thymidine uptake (TU) by various normal cell types, including activated lymphocytes. It has been postulated that this apparent antiproliferative effect may play an in vivo role in the high tumorigenic capacity of SV40-transformed hamster cells. In keeping with this hypothesis, Adenovirus type 2-transformed hamster cells, which are only weakly tumorigenic, do not inhibit TU by indicator cells in vitro. To study the biological relevance of this phenomenon, we assayed 11 cell lines derived from different fibrosarcomas, induced in Syrian hamsters by SV40, for their ability to inhibit TU by normal rabbit kidney indicator cells. In contrast to cells transformed in vitro by SV40, media conditioned by 6 of 11 tumor-derived cell lines did not inhibit TU. Our results do not support the hypothesis that an antiproliferative factor secreted by SV40-transformed cells promotes the tumor-inducing capacity of these cells. Furthermore, inhibition of TU does not appear to be due to the production of a specific antimitotic peptide, but rather to other biochemical properties of the media conditioned by transformed cells. Finally, these biochemical properties do appear to correlate with specific morphological and growth characteristics of the tumor cells, but probably as an effect and not a cause.
据报道，经SV40体外转化的仓鼠细胞会分泌一种不明因子，该因子能抑制包括活化淋巴细胞在内的多种正常细胞类型摄取胸苷（TU）。据推测，这种明显的抗增殖作用可能在SV40转化的仓鼠细胞的高致瘤能力中发挥体内作用。与这一假设相符的是，2型腺病毒转化的仓鼠细胞致瘤性较弱，在体外不会抑制指示细胞摄取胸苷。为了研究这一现象的生物学相关性，我们检测了11种源自叙利亚仓鼠经SV40诱导产生的不同纤维肉瘤的细胞系抑制正常兔肾指示细胞摄取胸苷的能力。与经SV40体外转化的细胞不同，11种肿瘤来源的细胞系中有6种的条件培养基不会抑制胸苷摄取。我们的结果不支持以下假设：SV40转化细胞分泌的抗增殖因子会促进这些细胞的致瘤能力。此外，胸苷摄取的抑制似乎并非由于产生了特定的抗有丝分裂肽，而是由于转化细胞条件培养基的其他生化特性。最后，这些生化特性似乎确实与肿瘤细胞的特定形态和生长特征相关，但可能是一种效应而非原因。
