Joly-Pharaboz M O, Albaladejo V, Morel Y, Trouillas J, Andre J
INSERM-U.34, UER Lyon Nord, Hôpital Debrousse, France.
J Steroid Biochem. 1988;30(1-6):369-73. doi: 10.1016/0022-4731(88)90125-2.
It is known that estradiol, but not progesterone or dihydrotestosterone, slows down the growth of the MtTF4 tumor. In the present paper, it is shown that: (1) this tumor contains glucocorticoid receptors, (2) its growth is also inhibited by treatment with dexamethasone (Dex), and (3) the growth rate of a cell line and several clones established from the tumor is negatively controlled by Dex 10(-7) M in culture medium containing 10% gelding serum. Unlike estradiol, Dex does not induce cell hypertrophy. This work suggests that the inhibition of the MtTF4 tumor growth by Dex may be due in part to a direct action on tumor cells and, taking into consideration previous reports, it allows us to forward the hypothesis that both Dex and estradiol inhibit MtTF4 tumor growth in two different ways.
已知雌二醇可减缓MtTF4肿瘤的生长,而孕酮或双氢睾酮则无此作用。在本论文中,研究表明:(1)该肿瘤含有糖皮质激素受体;(2)地塞米松(Dex)处理也可抑制其生长;(3)在含有10%马血清的培养基中,由该肿瘤建立的细胞系及多个克隆的生长速率受到10⁻⁷ M Dex的负调控。与雌二醇不同,Dex不会诱导细胞肥大。这项研究表明,Dex对MtTF4肿瘤生长的抑制作用可能部分归因于对肿瘤细胞的直接作用,结合先前的报道,这使我们提出假说,即Dex和雌二醇以两种不同方式抑制MtTF4肿瘤生长。