Descending-SHIP2-mediated radiosensitivity enhancement through PI3K/Akt signaling pathway in laryngeal squamous cell carcinoma - 18/09/19
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Graphical abstract |
Highlights |
• | SHIP2 knockdown can impair the proliferation, invasion and migration and promote the apoptosis in LSCC. |
• | Radiation can suppress SHIP2 expression and cause a similar effect to SHIP2 knockdwon on LSCC. |
• | Descending SHIP2 expression mediate enhanced radiosensitivity via PI3K/Akt signaling pathway. |
Abstract |
Laryngeal squamous cell carcinoma (LSCC) is the major type of laryngeal carcinoma. SHIP2 plays a critical role in malignant tumors and is associated with activation of PI3K/Akt signaling pathway. Here, we aimed to explore the impacts of SHIP2 on LSCC Hep-2 cells and the relationship between SHIP2 and radiotherapy. SHIP2 knockdown impairs cell proliferation, invasion, migration and promotes cell apoptosis in this study, suggesting the oncogenic role of SHIP2 in laryngeal cancer. Radiation not only has the similar effect on laryngeal cancer as SHIP2 knockdown, but also causes significant cell cycle G2 arrest, all of which can be significantly enhanced by SHIP2 knockdown. This enhancement effect cause by SHIP2 knockdown derive from the inactivation of PI3K/Akt signaling pathway along with its downstream proteins. Our finding revealed a novel mechanism for sensitivity to radiotherapy caused by SHIP2 knockdown that called descending-SHIP2-mediated radiosensitivity enhancement (DSMRSE).
Le texte complet de cet article est disponible en PDF.Keywords : Descending-SHIP2-mediated radiosensitivity enhancement, Laryngeal squamous cell carcinoma, SHIP2, PI3K/Akt, pAKT, Radiosensitivity
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Vol 118
Article 109392- octobre 2019 Retour au numéro
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