Knockdown of inhibitor of differentiation 1 suppresses proliferation and induces apoptosis by inactivating PI3K/Akt/mTOR signaling in hemangioma-derived endothelial cells - 16/02/19
, Hongzhao Lei a, Yubin Gong a, Miaomiao Li a, Yuanfang Zhang a, Hongyu Zhang a, Longlong Sun bBienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
Highlights |
• | ID-1 expression was upregulated in HDECs. |
• | Knockdown of ID-1 inhibited the proliferation of HDECs. |
• | Knockdown of ID-1 induced apoptosis of HDECs. |
• | Knockdown of ID-1 inactivated the PI3K/Akt/mTOR pathway. |
Abstract |
Hemangioma (HA) is one of the commonest benign vascular neoplasms of infancy. Inhibitor of differentiation 1 (ID-1) has been reported to be an oncogene in multiple cancers. However, the role of ID-1 and its molecular mechanism in HA progression have not been elucidated. In the present study, we found that ID-1 expression at mRNA and protein levels was up-regulated in HA-derived endothelial cells (HDECs). Knockdown of ID-1 inhibited proliferation, facilitated apoptosis, and enhanced propranolol cytotoxicity in HDECs. Knockdown of ID-1 decreased the protein levels of phospholyrated protein kinase-B (Akt) and phospholyrated mammalian target of rapamycin (mTOR). Inhibition of PI3K/Akt/mTOR pathway by LY294002 abrogated ID-1-mediated pro-proliferation and anti-apoptosis effects in HDECs. In conclusion, knockdown of ID-1 suppressed proliferation and promoted apoptosis by inactivating phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR signaling in HDECs, shedding light on the function of ID-1 in HA progression and highlighting the therapeutic value of ID-1 for HA.
Le texte complet de cet article est disponible en PDF.Keywords : Hemangioma, ID-1, PI3K/Akt/mTOR, Proliferation, Apoptosis
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Vol 111
P. 236-243 - mars 2019 Retour au numéro
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