Goya L, Edwards C P, Glennemeier K A, Firestone G L
Department of Molecular and Cell Biology, University of California at Berkeley 94720.
Cancer Lett. 1991 Jul 4;58(3):211-9. doi: 10.1016/0304-3835(91)90103-o.
We have previously demonstrated that BDS.1 cells are a minimal deviation rat hepatoma cell line that is hypersensitive to the anti-proliferative effects of glucocorticoids in vitro. When transplanted into athymic mice, exposure to dexamethasone reduced the initial growth rate and increased the latency time before detection of palpable BDS.1-derived tumors but did not affect the maximal growth rate, size and histology of the tumor. After collagenase dissociation, the in vitro growth of BDS.1-derived tumor cells was fully suppressed by dexamethasone. Exposure to insulin prevented the glucocorticoid inhibition of anchorage-independent growth of BDS.1 cell colonies in vitro and may therefore be one of the systemic factors that masks the long term in vivo growth response of glucocorticoids.
我们之前已经证明,BDS.1细胞是一种微小偏离型大鼠肝癌细胞系,在体外对糖皮质激素的抗增殖作用高度敏感。当将其移植到无胸腺小鼠体内时,地塞米松的作用会降低其初始生长速率,并延长可触及的源自BDS.1的肿瘤被检测到之前的潜伏期,但不影响肿瘤的最大生长速率、大小和组织学。胶原酶解离后,地塞米松可完全抑制源自BDS.1的肿瘤细胞的体外生长。胰岛素的作用可防止糖皮质激素对BDS.1细胞集落体外非锚定依赖性生长的抑制,因此可能是掩盖糖皮质激素体内长期生长反应的全身因素之一。