Nakano A, Tani E, Miyazaki K, Yamamoto Y, Furuyama J
Department of Neurosurgery, Hyogo College of Medicine, Japan.
J Neurosurg. 1995 Aug;83(2):298-307. doi: 10.3171/jns.1995.83.2.0298.
The gene expression of five matrix metalloproteinases (MMPs) and two tissue inhibitors of metalloproteinases (TIMPs) was studied in human gliomas in vivo and in vitro to evaluate their roles in glioma invasion. Simultaneous expression of one to four MMP genes and two TIMP genes was found in 17 surgical glioma specimens, and one MMP (gelatinase A) gene and two TIMP genes were simultaneously expressed in tissue of three brains. The concomitant overexpression of gelatinase A, gelatinase B, and occasional matrilysin genes was associated with the malignancy of gliomas and accompanied by overexpression of the TIMP-1 gene. In five human glioma cell lines, gelatinase A, TIMP-1, and TIMP-2 genes were constitutively expressed in alll cell lines: the matrilysin gene in three cell lines; the stromelysin gene in two cell lines; and the interstitial collagenase gene in one cell line. There was a clear difference in the expression of gelatinase B and stromelysin genes between surgical glioma specimens and glioma cell lines: the gelatinase B gene was not expressed constitutively in vitro but was overexpressed in vivo, whereas the stromelysin gene was not expressed in vivo but was expressed in some cell lines. To find the cause of that difference in vivo and in vitro, the transcriptional regulations of MMP and TIMP genes by tumor promoter, growth factors, or cytokines were studied in vitro. Interstitial collagenase, gelatinase B, stromelysin, and TIMP-1 genes were upregulated in many cell lines by phorbol-12-myristate-13-acetate (PMA) and in some cell lines by epidermal growth factor, tumor necrosis factor-alpha, or interleukin-1 beta. Transforming growth factor-beta 1 (TGF beta 1) upregulated gelatinase A and matrilysin genes in some cell lines, and there were no clear responses from any MMP and TIMP genes to interleukin-6. Thus, the transcriptional modulation of MMP genes by these growth factors and cytokines seemed insufficient to explain the difference in gelatinase B and stromelysin gene expressions in vivo and in vitro and was suggestive of the genetic alteration of glioma cells in vitro, the heterogeneous cell population in glioma tissues, or both. Furthermore, the in vitro invasion of glioma cells through Matrigel in response to PMA, TGF beta 1, or TIMP-1 was assessed by chemoinvasion assay. In most cell lines, invasion was significantly stimulated by PMA or TGF beta 1 but suppressed by TIMP-1.(ABSTRACT TRUNCATED AT 400 WORDS)
为评估五种基质金属蛋白酶(MMPs)和两种金属蛋白酶组织抑制剂(TIMPs)在神经胶质瘤侵袭中的作用,对其在体内和体外的人神经胶质瘤中的基因表达进行了研究。在17个手术切除的神经胶质瘤标本中发现了1至4个MMP基因和2个TIMP基因的同时表达,并且在三个脑的组织中同时表达了一个MMP(明胶酶A)基因和2个TIMP基因。明胶酶A、明胶酶B以及偶尔的基质溶素基因的伴随过表达与神经胶质瘤的恶性程度相关,并伴有TIMP-1基因的过表达。在五个人神经胶质瘤细胞系中,明胶酶A、TIMP-1和TIMP-2基因在所有细胞系中均组成性表达:基质溶素基因在三个细胞系中表达;基质溶解素基因在两个细胞系中表达;间质胶原酶基因在一个细胞系中表达。手术切除的神经胶质瘤标本和神经胶质瘤细胞系之间明胶酶B和基质溶解素基因的表达存在明显差异:明胶酶B基因在体外不是组成性表达,但在体内过表达,而基质溶解素基因在体内不表达,但在一些细胞系中表达。为了找出体内和体外这种差异的原因,在体外研究了肿瘤启动子、生长因子或细胞因子对MMP和TIMP基因的转录调控。在许多细胞系中,佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)上调了间质胶原酶、明胶酶B、基质溶解素和TIMP-1基因,在一些细胞系中,表皮生长因子、肿瘤坏死因子-α或白细胞介素-1β上调了这些基因。转化生长因子-β1(TGFβ1)在一些细胞系中上调了明胶酶A和基质溶素基因,并且任何MMP和TIMP基因对白细胞介素-6均无明显反应。因此,这些生长因子和细胞因子对MMP基因的转录调节似乎不足以解释体内和体外明胶酶B和基质溶解素基因表达的差异,这提示了体外神经胶质瘤细胞的基因改变、神经胶质瘤组织中细胞群体的异质性或两者皆有。此外,通过化学侵袭试验评估了神经胶质瘤细胞在体外对PMA、TGFβ1或TIMP-1的穿过基质胶的侵袭能力。在大多数细胞系中,PMA或TGFβ1显著刺激侵袭,但TIMP-1抑制侵袭。(摘要截短于400字)