Constitutive expression and secretion of proteases in non-metastatic SP1 mammary carcinoma cells and its metastatic sublines.
Constitutive expression and secretion of proteases in non-metastatic SP1 mammary carcinoma cells and its metastatic sublines.
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非转移性 SP1 乳腺癌细胞及其转移性亚系中蛋白酶的组成型表达和分泌。
DOI:
10.1002/ijc.2910480413
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发表时间:
1991
影响因子:
6.4
通讯作者:
Dennis,J
中科院分区:
文献类型:
--
作者:
Korczak,B;Kerbel,RS;Dennis,J
Malignant tumors are generally characterized by extensive local tissue invasion and destruction of ECM which may be due to increased constitutive expression and activity of secreted proteases. Moreover, a large number of diverse protease activities may be constitutively over‐expressed in a simultaneous or co‐ordinated fashion, thereby significantly increasing cellular invasive potential of the cells. To explore this relationship, we have measured steady‐state levels of mRNA coding for uroklnase plasminogen activator (uPA), tissue plasminogen activator (tPA), transin and tissue‐specific inhibitor of metalloproteinases (TIMP); as well as gelatinolytic, caseinolytic and plasminogen activator activities secreted by SPI, a non‐metastatic mouse mammary carcinoma cell line and 4 metastatic sublines derived from it. mRNA encoding metalloproteinase transin was increased 15‐ to 20‐fold, while TIMP transcripts were decreased 3‐fold in the metastatic sublines compared to parental SPI tumor cells. Metastatic sublines secreted higher levels of gelatinase (i.e., 92 kDa and 64 kDa) as well as proteases with caseinolytic activity (i.e., 115 kDa and 57 kDa) when compared with SPI cells. Moreover, these enzymes were identified as neutral metalloproteinases. Although the amount of uPA mRNA appeared to be the same in SPI and the metastatic sublines, the latter secreted 1.5–3 times more uPA activity into the culture supernatants. Metastatic competence in the SPI tumor model is therefore associated with increased secretion of several metalloproteinase activities and uPA, as well as decreased TIMP expression, consistent with a more invasive phenotype.
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影响因子:
64.5
作者:
MIGNATTI, P;ROBBINS, E;RIFKIN, DB
通讯作者:
RIFKIN, DB
DOI:
10.1016/0006-291x(87)90463-3
发表时间:
1987
影响因子:
3.1
作者:
Karlan,BY;Clark,AS;Littlefield,BA
通讯作者:
Littlefield,BA
影响因子:
11.2
作者:
Allen,LE;Dubeau,L;Alvarez,O;Jones,PA
通讯作者:
Jones,PA
DOI:
10.1073/pnas.84.19.6725
发表时间:
1987
影响因子:
11.1
作者:
Wilhelm,SM;Collier,IE;Kronberger,A;Eisen,AZ;Marmer,BL;Grant,GA;Bauer,EA;Goldberg,GI
通讯作者:
Goldberg,GI
DOI:
10.1056/nejm197705052961801
发表时间:
1977
期刊:
The New England journal of medicine
影响因子:
--
作者:
Z. Werb;C. Mainardi;C. Vater;E. D. Harris
通讯作者:
E. D. Harris