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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mullerian inhibiting substance suppresses tumor growth in the C3(1)T antigen transgenic mouse mammary carcinoma model
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Mullerian inhibiting substance suppresses tumor growth in the C3(1)T antigen transgenic mouse mammary carcinoma model

机译：苗勒霉抑制物质抑制C3（1）T抗原转基因小鼠乳腺癌模型中的肿瘤生长

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摘要

Mullerian inhibiting substance (MIS) inhibits breast cancer cell growth in vitro. To extend the use of MIS to treat breast cancer, it is essential to test the responsiveness of mammary tumor growth to MIS in vivo. Mammary tumors arising in the C3(1) T antigen mouse model expressed the MIS type Ⅱ receptor, and MIS in vitro inhibited the growth of cells derived from tumors. Administration of MIS to mice was associated with a lower number of palpable mammary tumors compared with vehicle-treated mice (P = 0.048), and the mean mammary tumor weight in the MIS-treated group was significantly lower compared with the control group (P = 0.029). Analysis of proliferating cell nuclear antigen (PCNA) expression and caspase-3 cleavage in tumors revealed that exposure to MIS was associated with decreased proliferation and increased apoptosis, respectively, and was not caused by a decline in T antigen expression. The effect of MIS on tumor growth was also evaluated on xenografted human breast cancer cell line MDA-MB-468, which is estrogen receptor- and retinoblastoma-negative and expresses mutant p53, and thus complements the C3(1)Tag mouse mammary tumors that do not express estrogen receptor and have functional inactivation of retinoblastoma and p53. In agreement with results observed in the transgenic mice, MIS decreased the rate of MDA-MB-468 tumor growth and the gain in mean tumor volume in severe combined immunodeficient mice compared with vehicle-treated controls (P = 0.004). These results suggest that MIS can suppress the growth of mammary tumors in vivo.
机译：苗勒氏抑制物质（MIS）在体外抑制乳腺癌细胞的生长。为了扩展MIS的使用来治疗乳腺癌，必须在体内测试乳腺肿瘤生长对MIS的反应性。 C3（1）T抗原小鼠模型中出现的乳腺肿瘤表达了MIS II型受体，而MIS在体外抑制了肿瘤细胞的生长。与赋形剂治疗的小鼠相比，对小鼠施用MIS与可触及的乳腺肿瘤数量较少（P = 0.048），而与对照组相比，MIS治疗组的平均乳腺肿瘤重量明显更低（P = 0.029）。对肿瘤中增殖细胞核抗原（PCNA）表达和caspase-3裂解的分析表明，暴露于MIS分别与增殖减少和凋亡增加有关，而不是由T抗原表达的下降引起的。还对异种移植的人类乳腺癌细胞系MDA-MB-468评估了MIS对肿瘤生长的影响，该细胞系雌激素受体和视网膜母细胞瘤阴性，并表达突变型p53，从而补充了C3（1）Tag小鼠乳腺肿瘤，不表达雌激素受体，并具有视网膜母细胞瘤和p53的功能失活。与在转基因小鼠中观察到的结果一致，与媒介物处理的对照组相比，MIS降低了重度合并免疫缺陷小鼠中MDA-MB-468肿瘤的生长速度和平均肿瘤体积的增加（P = 0.004）。这些结果表明MIS可以在体内抑制乳腺肿瘤的生长。

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