McGrath C M, Jones R F
Cancer Res. 1978 Nov;38(11 Pt 2):4112-25.
The purpose of this study was to evaluate the possibility that hormones and mouse mammary tumor virus (MuMTV) are cocarcinogenic for mammary epithelium. Results of our investigations in vivo and in vitro suggest: (a) Hormones promote mammary carcinogenesis in BALB/c females whether MuMTV is germinally (BALB/c) or horizontally (BALB/cfC3H) transmitted; the rate of carcinogenesis in BALB/cfC3H females is substantially faster than it is in BALB/c, but the final mammary carcinoma incidence is approximately the same. The rate-limiting step in malignant transformation in BALB/c, which infectious MuMTV overcomes, is in premalignant transformation from normal. (b) One characteristic of horizontal MuMTV transmission in BALB/c that is not observed in germinal transmission is integration of new MuMTV sequences in mammary cell DNA. Integration is mammary cell specific and constant at 2 to 3 copies/cell from tumor to tumor. (c) MuMTV expression is changed in mammary epithelial cells during hormonal carcinogenesis. The nature of the change is qualitatively similar in both BALB/c and BALB/cfC3H. Expression of envelope glycopeptides (glycoprotein with a molecular weight of 52,000) is induced, which correlates with amplification of MuMTV RNA sequence content. Quantitative differences exist in induced levels in BALB/c and BALB/cfC3H. (d) MuMTV RNA and a glycoprotein with a molecular weight of 52,000 were not inducible with dexamethasone in normal mammary epithelial cells in culture. These structural components were induced in both premalignant (BALB/cfC3H) and malignant (BALB/c and BALB/cfC3H) cells. MuMTV RNA was induced by dexamethasone in normal cells pretreated with 5-iodo-2'-deoxyuridine. (e) Both premalignant and malignant cells have altered (vis-à-vis normal) surfaces, discernible by differences in reactivity with concanavalin A in hemadsorption assays. Indirect evidence suggests that the alteration includes membrane incorporation of MuMTV-related determinants of a glycoprotein with a molecular weight of 52,000. (f) Malignant cells exhibit enhanced sensitivity to insulin for reinitiation of DNA synthesis and mitosis in contact-inhibited homotypical monolayers. These findings have been organized into a hormonal cocarcinogenesis hypothesis in which expression of germinally transmitted MuMTV genes is the proximal cause of neoplastic transformation.
本研究的目的是评估激素与小鼠乳腺肿瘤病毒(MuMTV)对乳腺上皮细胞是否具有协同致癌作用。我们在体内和体外的研究结果表明:(a)无论MuMTV是通过种系(BALB/c)还是水平(BALB/cfC3H)传播,激素均可促进BALB/c雌性小鼠的乳腺癌发生;BALB/cfC3H雌性小鼠的致癌速率明显快于BALB/c,但最终乳腺癌的发病率大致相同。在BALB/c小鼠中,感染性MuMTV克服的恶性转化限速步骤是从正常细胞到癌前细胞的转化。(b)在BALB/c小鼠中,水平传播的MuMTV有一个在种系传播中未观察到的特征,即新的MuMTV序列整合到乳腺细胞DNA中。整合具有乳腺细胞特异性,每个肿瘤细胞中的整合拷贝数恒定为2至3个。(c)在激素致癌过程中,乳腺上皮细胞中MuMTV的表达发生了变化。在BALB/c和BALB/cfC3H中,这种变化的性质在定性上是相似的。包膜糖肽(分子量为52,000的糖蛋白)的表达被诱导,这与MuMTV RNA序列含量的扩增相关。在BALB/c和BALB/cfC3H中,诱导水平存在定量差异。(d)在培养的正常乳腺上皮细胞中,地塞米松不能诱导MuMTV RNA和分子量为52,000的糖蛋白。在癌前(BALB/cfC3H)和恶性(BALB/c和BALB/cfC3H)细胞中均可诱导这些结构成分。在用5-碘-2'-脱氧尿苷预处理的正常细胞中,地塞米松可诱导MuMTV RNA。(e)癌前细胞和恶性细胞的表面(相对于正常细胞)均发生了改变,这在血细胞吸附试验中通过与伴刀豆球蛋白A反应性的差异得以辨别。间接证据表明,这种改变包括分子量为52,000的糖蛋白的MuMTV相关决定簇掺入细胞膜。(f)在接触抑制的同型单层细胞中,恶性细胞对胰岛素重新启动DNA合成和有丝分裂表现出更高的敏感性。这些发现已被整合为一个激素协同致癌假说,其中种系传播的MuMTV基因的表达是肿瘤转化的近端原因。