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首页> 外文期刊>Journal of Cellular Physiology >New signaling pathways from cancer progression modulators to mRNA expression of matrix metalloproteinases in breast cancer cells.
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New signaling pathways from cancer progression modulators to mRNA expression of matrix metalloproteinases in breast cancer cells.

机译：新癌症恶化的信号通路调节器的mRNA表达矩阵金属蛋白酶在乳腺癌细胞。

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摘要

We observed previously that each of seven cancer progression inhibitors suppresses the mRNA expression of some matrix metalloproteinases (MMPs), but stimulates that of others, in breast cancer cells. In the present study we tested the effect of overexpressing other cancer modulators on MMP expression. The MMPs tested are MMP1, MMP2, MMP7, MMP13, MMP14, MMP16, MMP19, and MMP25. The proteins that were overexpressed are cancer inhibitors (NME, DRG1, IL10), enhancers (SOD2, FAK, IL17, and CREB), and proteins that suppress cancer progression in cells of some cancers and promote it in others (FUT1, integrin beta3, serpin E1, TIAM1, and claudin 4). Unexpectedly, all of them only lowered MMP mRNA expression, mainly of MMP16, MMP2, and MMP13, in breast cancer cells. Signaling from SOD2 uncoupled the accumulation of two MMP16 mRNA splice variants, suggesting signaling to a late step in MMP16 mRNA accumulation, such as MMP16 mRNA stabilization or late mRNA processing. Signaling that modulates MMP expression differed widely among the total population of MDA-MB-231 cells and single-cell progenies cloned from that population. It also differed substantially between cells of two metastatic breast basal adenocarcinomas, MDA-MB-231 and MDA-MB-468. The present study detected 37 new signaling pathways from cancer progression modulators located upstream of MMP mRNA expression in human breast cancer cells. Our siRNA-induced MMP knockdown data support the interpretation that signaling from MMP19, MMP1, MMP7, MMP12, MMP14, and MMP11 each stimulates the mRNA expression of other MMPs in breast cancer cells.
机译：我们观察到以前的七个癌症进展抑制剂抑制mRNA基质金属蛋白酶的表达(基质金属蛋白酶),但在乳房刺激别人,癌细胞。overexpressing其他癌症调节器的效果MMP的表达。MMP2、MMP7 MMP13、MMP14 MMP16 MMP19,MMP25。癌症抑制剂(NME DRG1 IL10),增强剂(SOD2 FAK IL17和分子),和蛋白质抑制癌症细胞的一些进展癌症和促进它在其他(FUT1,整合素beta3, serpin E1、TIAM1 claudin 4)。出乎意料,他们只有降低MMP的信使rna主要表达,MMP16, MMP2, MMP13,乳腺癌细胞。分开两个MMP16信使rna的积累后期剪接变体,暗示信号一步MMP16 mRNA积累,比如MMP16信使rna稳定或迟mRNA加工。信号,调节MMP的表达不同广泛的总人口中mda - mb - 231细胞和单细胞克隆后代人口。两个转移性乳腺癌细胞基底之间腺癌,mda - mb - 231和mda - mb - 468。本研究发现37个新的信号通路从癌症恶化调节器在人类乳房上游MMP的mRNA表达癌细胞。数据支持信号的解释从MMP19 MMP1、MMP7 MMP12 MMP14, MMP11每个刺激其他的mRNA表达基质金属蛋白酶在乳腺癌细胞。

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