EXPRESSION OF GELATINASE-A AND TIMP-2 MESSENGER-RNAS IN DESMOPLASTIC FIBROBLASTS IN BOTH MAMMARY CARCINOMAS AND BASAL-CELL CARCINOMAS OF THE SKIN
EXPRESSION OF GELATINASE-A AND TIMP-2 MESSENGER-RNAS IN DESMOPLASTIC FIBROBLASTS IN BOTH MAMMARY CARCINOMAS AND BASAL-CELL CARCINOMAS OF THE SKIN
复制标题
DOI：
10.1136/jcp.46.5.429
复制
发表时间：
1993-05-01
影响因子：
3.4
通讯作者：
STAMP, GWH
中科院分区：
文献类型：
--
作者：
POULSOM, R;HANBY, AM;STAMP, GWH
目的-比较基底膜降解酶明胶酶A的mRNA定位（72千道尔顿IV型胶原酶）及其抑制剂TIMP-2在乳腺癌和具有很少或没有转移能力的皮肤基底细胞癌中的应用。三个纤维腺瘤，和良性叶状肿瘤，和15基底细胞癌的皮肤（BCC）。结果标记的mRNA是可检测的14 16个乳腺癌和13 15 BCC，最经常超过组织促纤维增生成纤维细胞周围的浸润性上皮细胞聚集的基质。一些稀疏的标记被认为是恶性上皮细胞在6个乳腺癌，但不是在基底细胞癌。明胶酶A mRNA的一些表达也见于乳腺癌附近乳腺小叶的成纤维细胞和BCC中被吞噬的附件元件周围，但在未受影响的乳腺组织、纤维腺瘤、叶状肿瘤或未受影响的皮肤。结论明胶酶A和TIMP的最大表达-2 mRNA在恶性肿瘤中作为宿主对已建立的肿瘤细胞存在的反应的一部分而不是作为对侵袭的初始反应。这种存在的程度表明这可能是调节肿瘤分化、生长和进展的高度相关机制，可能需要通过肿瘤细胞表面上的特异性受体摄取。
Aims-To compare the localisation of mRNAs for the basement membrane degrading enzyme gelatinase A (72 kilodalton type IV collagenase) and its inhibitor TIMP-2 in carcinomas of the breast and basal cell carcinomas of the skin which have little or no ability to metastasise.Methods-In situ hybridisation was performed on formalin fixed, paraffin wax embedded blocks using S-35-labelled riboprobes on 16 mammary carcinomas, three fibroadenomas, and a benign phyllodes tumour, and on 15 basal cell carcinomas of the skin (BCC).Results-Labelling for both mRNAs was detectable in 14 of 16 mammary carcinomas and in 13 of 15 BCC, most often over organising desmoplastic fibroblasts in the stroma around invasive epithelial aggregates. Some sparse labelling was seen over malignant epithelial cells in six of the mammary carcinomas but not in the BCC. Some expression of gelatinase A mRNA was also seen in fibroblasts of breast lobules adjacent to the mammary carcinomas and around engulfed adnexal elements in the BCC, but not in unaffected breast tissues, fibroadenomas, the phyllodes tumour or unaffected skin.Conclusions-Maximal expression of gelatinase A and TIMP-2 mRNAs occurs in malignant neoplasms as part of the host response to the presence of established neoplastic cells rather than as an initial response to invasion. The degree to which this is present suggests this may be a highly relevant mechanism modulating tumour differentiation, growth and progression, possibly entailing uptake via specific receptors on the tumour cell surface.