Carrera M P, Ramírez-Expósito M J, Valenzuela M T, García M J, Mayas M D, Arias de Saavedra J M, Sánchez R, Pérez M C, Martínez-Martos J M
Departamento de Ciencias de la Salud, Area de Fisiología, Universidad de Jaén, Campus Universitario Las Lagunillas, 23071 Jaén, Spain.
Horm Metab Res. 2005 Feb;37(2):74-8. doi: 10.1055/s-2005-861158.
Pyrrolidon carboxypeptidase is an omega-peptidase that hydrolyses N-terminal pyroglutamyl residues from biologically active peptides such as gonadotropin-releasing and thyrotrophin-releasing hormones. We previously described a decrease in both rat and human pyrrolidon carboxypeptidase activity with breast cancer, suggesting that gonadotropin-releasing hormone may be an important local intracrine, autocrine and/or paracrine hormonal factor in the pathogenesis of breast cancer while playing a role in the tumoral process. However, the other susceptible substrate of pyrrolidon carboxypeptidase, thyrotrophin-releasing hormone, may also be modified with breast cancer, supporting an association between breast cancer and thyroid disorders. The present work analyses soluble and membrane-bound pyrrolidon carboxypeptidase activities in the hypothalamus-pituitary-thyroid and hypothalamus-pituitary-ovary axes in N-methyl nitrosourea-induced breast cancer in rats. Our aim was to determine the possible relationship between gonadotropin-releasing hormone and thyrotrophin-releasing hormone regulation through pyrrolidon carboxypeptidase activity. We propose that pyrrolidon carboxypeptidase activity dysregulation at various local and systemic levels may participate in the initiation, promotion and progression of breast cancer induced in rat by N-methyl nitrosourea through the increase in gonadotropin-releasing hormone. Since pyrrolidon carboxypeptidase activity also acts on thyrotrophin-releasing hormone, the dysregulation of this enzyme's activity could indirectly affect hypothalamus-pituitary-thyroid axis function, and thus potentially represent a link between the diseases of thyroid and breast cancer.
吡咯烷酮羧肽酶是一种ω-肽酶,可从生物活性肽(如促性腺激素释放激素和促甲状腺激素释放激素)中水解N端焦谷氨酰残基。我们之前描述过,大鼠和人类的吡咯烷酮羧肽酶活性在乳腺癌中均下降,这表明促性腺激素释放激素可能是乳腺癌发病机制中的一种重要的局部内分泌、自分泌和/或旁分泌激素因子,同时在肿瘤过程中发挥作用。然而,吡咯烷酮羧肽酶的另一种敏感底物促甲状腺激素释放激素,也可能因乳腺癌而发生改变,这支持了乳腺癌与甲状腺疾病之间的关联。本研究分析了N-甲基亚硝基脲诱导的大鼠乳腺癌模型中,下丘脑-垂体-甲状腺轴和下丘脑-垂体-卵巢轴中可溶性和膜结合型吡咯烷酮羧肽酶的活性。我们的目的是通过吡咯烷酮羧肽酶活性来确定促性腺激素释放激素和促甲状腺激素释放激素调节之间的可能关系。我们提出,在各种局部和全身水平上,吡咯烷酮羧肽酶活性失调可能通过促性腺激素释放激素的增加,参与N-甲基亚硝基脲诱导的大鼠乳腺癌的起始、促进和进展过程。由于吡咯烷酮羧肽酶活性也作用于促甲状腺激素释放激素,这种酶活性的失调可能间接影响下丘脑-垂体-甲状腺轴的功能,因此可能代表甲状腺疾病和乳腺癌之间的一种联系。