GHOSH, Somadri, Samuel SCOZZARO, Ana Raque RAMOS, Seprimebastien DELCAMBRE, Cleprimement CHEVALIER, Pavel KREJČÍ and Christophe ERNEUX. Inhibition of SHIP2 activity inhibits cell migration and could prevent metastasis in breast cancer cells. Journal of Cell Science. Cambridge: Company of Biologists Ltd., 2018, vol. 131, No 16, p. 1-12. ISSN 0021-9533. Available from: https://dx.doi.org/10.1242/jcs.216408.
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Basic information
Original name Inhibition of SHIP2 activity inhibits cell migration and could prevent metastasis in breast cancer cells
Authors GHOSH, Somadri (56 Belgium), Samuel SCOZZARO (56 Belgium), Ana Raque RAMOS (56 Belgium), Seprimebastien DELCAMBRE (56 Belgium), Cleprimement CHEVALIER (56 Belgium), Pavel KREJČÍ (203 Czech Republic, belonging to the institution) and Christophe ERNEUX (56 Belgium, guarantor).
Edition Journal of Cell Science, Cambridge, Company of Biologists Ltd. 2018, 0021-9533.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 4.517
RIV identification code RIV/00216224:14110/18:00104188
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1242/jcs.216408
UT WoS 000443438900007
Keywords in English SHIP2; Phosphoinositide; Cell migration; Breast cancer cell
Tags 14110513, rivok
Tags International impact, Reviewed
Changed by Changed by: Soňa Böhmová, učo 232884. Changed: 10/2/2019 14:56.
Abstract
Metastasis of breast cancer cells to distant organs is responsible for similar to 50% of breast cancer-related deaths in women worldwide. SHIP2 (also known as INPPL1) is a phosphoinositide 5-phosphatase for phosphatidylinositol (3,4,5)-trisphosphate [PI(3,4,5)P3] and phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P2]. Here we show, through depletion of SHIP2 in triple negative MDA-MB-231 cells and the use of SHIP2 inhibitors, that cell migration appears to be positively controlled by SHIP2. The effect of SHIP2 on migration, as observed in MDA-MB-231 cells, appears to be mediated by PI(3,4) P2. Adhesion on fibronectin is always increased in SHIP2-depleted cells. Apoptosis measured in MDA-MB-231 cells is also increased in SHIP2-depleted cells as compared to control cells. In xenograft mice, SHIP2-depleted MDA-MB-231 cells form significantly smaller tumors than those formed by control cells and less metastasis is detected in lung sections. Our data reveal a general role for SHIP2 in the control of cell migration in breast cancer cells and a second messenger role for PI(3,4) P2 in the migration mechanism. In MDA-MB-231 cells, SHIP2 has a function in apoptosis in cells incubated in vitro and in mouse tumor-derived cells, which could account for its role on tumor growth determined in vivo.
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