Mokyr M B, Przepiorka D, Dray S
Cancer Res. 1982 Jul;42(7):2537-43.
Some of the possible mechanisms by which polyethylene glycol (PEG) augments the ability of MOPC-315 tumor bearer spleen cells to mediate in vitro antitumor cytotoxicity were evaluated. The level of antitumor cytotoxicity obtained in 5-day cultures of tumor bearer spleen cell suspensions correlated inversely with the percentage of Trinitrophenol (TNP)-rosettable cells (presumably metastatic tumor cells) present in the spleen. The kinetics of decrease in the percentage of TNP-rosettable cells coincided with the appearance of antitumor cytotoxicity. In addition, PEG was shown to interfere with the ability of viable tumor cells to suppress the in vitro generation of antitumor cytotoxicity in normal spleen cells cultured with mitomycin C-treated tumor cells. However, the decrease in the content of TNP-rosettable cells and the concurrent increase in the level of antitumor cytotoxicity were not due to direct cytotoxic and/or cytostatic effects of PEG on tumor cells. Spleen cells cultured in the presence of PEG had an increased rate of [3H]thymidine incorporation and proliferation compared to spleen cells cultured in the absence of PEG. However, the PEG-induced decrease in the percentage of TNP-rosettable cells either preceded or occurred at the same time that the PEG-induced increase in spleen cell number was observed. Therefore, spleen cell proliferation can at best explain only partially the PEG-induced decrease in the content of TNP-rosettable cells, and other mechanisms for the decrease must be considered.
对聚乙二醇(PEG)增强MOPC - 315荷瘤小鼠脾细胞体外介导抗肿瘤细胞毒性能力的一些可能机制进行了评估。荷瘤小鼠脾细胞悬液5天培养物中获得的抗肿瘤细胞毒性水平与脾中可形成三硝基苯酚(TNP)玫瑰花结的细胞(可能是转移性肿瘤细胞)百分比呈负相关。TNP玫瑰花结形成细胞百分比的下降动力学与抗肿瘤细胞毒性的出现相吻合。此外,PEG被证明可干扰活肿瘤细胞抑制在用丝裂霉素C处理的肿瘤细胞培养的正常脾细胞中体外产生抗肿瘤细胞毒性的能力。然而,TNP玫瑰花结形成细胞含量的减少和抗肿瘤细胞毒性水平的同时增加并非由于PEG对肿瘤细胞的直接细胞毒性和/或细胞抑制作用。与在无PEG条件下培养的脾细胞相比,在PEG存在下培养的脾细胞[3H]胸腺嘧啶核苷掺入率和增殖率增加。然而,PEG诱导的TNP玫瑰花结形成细胞百分比的下降要么先于观察到的PEG诱导的脾细胞数量增加,要么与之同时发生。因此,脾细胞增殖充其量只能部分解释PEG诱导的TNP玫瑰花结形成细胞含量的下降,必须考虑其他导致下降的机制。