Hall M, Silverman L, Wenger A S, Mickey D D
Cancer Res. 1985 Sep;45(9):4053-9.
In this paper, data are presented which demonstrate that adenylate kinase and creatine kinase are oncodevelopmental enzymes in the rat prostate. The Dunning tumor (dorsal rat prostate) was used as a model system; four sublines of the tumor (R3327-H, R3327-AT, MAT Lu, and MAT LyLu) were studied. The tumor lines were maintained as solid tumors in syngeneic rats (Copenhagen) and as monolayers in tissue culture. The appearance of adenylate kinase with malignant transformation of the dorsal prostate was demonstrated. The disappearance of the CK-M subunit of creatine kinase and decreasing levels of creatine kinase were demonstrated with increasing anaplasia. The lactate dehydrogenase (LDH) concentration increased with increasing anaplasia, and the LDH isoenzyme pattern shifted to a more glycolytic pattern (LDH-4, LDH-5). The malignant isoenzyme pattern was reversible with the use of a differentiating agent (dimethyl sulfoxide). Prostates from neonatal rats and castrated adult male rats exhibited patterns of creatine kinase and adenylate kinase similar to those of the undifferentiated tumor. The oncofetal isoenzyme pattern of the castrated rat prostate was reversible with physiological levels of exogenous testosterone.
本文呈现的数据表明，腺苷酸激酶和肌酸激酶是大鼠前列腺中的肿瘤发育相关酶。邓宁肿瘤（大鼠背侧前列腺）被用作模型系统；研究了该肿瘤的四个亚系（R3327 - H、R3327 - AT、MAT Lu和MAT LyLu）。肿瘤系在同基因大鼠（哥本哈根大鼠）中维持为实体瘤，并在组织培养中维持为单层培养。证实了随着背侧前列腺的恶性转化，腺苷酸激酶出现。随着间变程度增加，肌酸激酶的CK - M亚基消失，肌酸激酶水平降低。乳酸脱氢酶（LDH）浓度随着间变程度增加而升高，且LDH同工酶谱向更具糖酵解特征的模式（LDH - 4、LDH - 5）转变。使用分化剂（二甲基亚砜）后，恶性同工酶谱是可逆的。新生大鼠和去势成年雄性大鼠的前列腺显示出与未分化肿瘤相似的肌酸激酶和腺苷酸激酶模式。去势大鼠前列腺的肿瘤胎儿同工酶谱在外源睾酮的生理水平作用下是可逆的。
