GHOSH, Somadri, Samuel SCOZZARO, Ana Raque RAMOS, Seprimebastien DELCAMBRE, Cleprimement CHEVALIER, Pavel KREJČÍ a 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, roč. 131, č. 16, s. 1-12. ISSN 0021-9533. Dostupné z: https://dx.doi.org/10.1242/jcs.216408.
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Základní údaje
Originální název Inhibition of SHIP2 activity inhibits cell migration and could prevent metastasis in breast cancer cells
Autoři GHOSH, Somadri (56 Belgie), Samuel SCOZZARO (56 Belgie), Ana Raque RAMOS (56 Belgie), Seprimebastien DELCAMBRE (56 Belgie), Cleprimement CHEVALIER (56 Belgie), Pavel KREJČÍ (203 Česká republika, domácí) a Christophe ERNEUX (56 Belgie, garant).
Vydání Journal of Cell Science, Cambridge, Company of Biologists Ltd. 2018, 0021-9533.
Další údaje
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor 10601 Cell biology
Stát vydavatele Velká Británie a Severní Irsko
Utajení není předmětem státního či obchodního tajemství
Impakt faktor Impact factor: 4.517
Kód RIV RIV/00216224:14110/18:00104188
Organizační jednotka Lékařská fakulta
Doi http://dx.doi.org/10.1242/jcs.216408
UT WoS 000443438900007
Klíčová slova anglicky SHIP2; Phosphoinositide; Cell migration; Breast cancer cell
Štítky 14110513, rivok
Příznaky Mezinárodní význam, Recenzováno
Změnil Změnila: Soňa Böhmová, učo 232884. Změněno: 10. 2. 2019 14:56.
Anotace
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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