ADAM9 silencing inhibits breast tumor cell invasion in vitro

ADAM9 (A Disintegrin And Metalloproteinase 9) is a member of the ADAM protein family which contains a disintegrin domain. This protein family plays key roles in many physiological processes, including fertilization, migration, and cell survival. The ADAM proteins have also been implicated in various...

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Published in:Biochimie Vol. 95; no. 7; pp. 1371 - 1378
Main Authors: Micocci, Kelli Cristina, Martin, Ana Carolina Baptista Moreno, Montenegro, Cyntia de Freitas, Durante, Araceli Cristina, Pouliot, Normand, Cominetti, Márcia Regina, Selistre-de-Araujo, Heloisa Sobreiro
Format: Journal Article
Language:English
Published: France Elsevier B.V 01-07-2013
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Summary:ADAM9 (A Disintegrin And Metalloproteinase 9) is a member of the ADAM protein family which contains a disintegrin domain. This protein family plays key roles in many physiological processes, including fertilization, migration, and cell survival. The ADAM proteins have also been implicated in various diseases, including cancer. Specifically, ADAM9 has been suggested to be involved in metastasis. To address this question, we generated ADAM9 knockdown clones of MDA-MB-231 breast tumor cells using silencing RNAs that were tested for cell adhesion, proliferation, migration and invasion assays. In RNAi-mediated ADAM9 silenced MDA-MB-231 cells, the expression of ADAM9 was lower from the third to the sixth day after silencing and inhibited tumor cell invasion in matrigel by approximately 72% when compared to control cells, without affecting cell adhesion, proliferation or migration. In conclusion, the generation of MDA-MB-231 knockdown clones lacking ADAM9 expression inhibited tumor cell invasion in vitro, suggesting that ADAM9 is an important molecule in the processes of invasion and metastasis. ► RNAi-mediated ADAM9 silencing inhibits MDA-MB-231 cell invasion. ► ADAM9 silencing had no effect on the migration or proliferation of MDA-MB-231 cells. ► ADAM9 can be a target for the design of drugs against breast cancer.
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ISSN:0300-9084
1638-6183
DOI:10.1016/j.biochi.2013.03.001