Activation autophagy contributes to non-apoptotic programmed cell death that facilitates the sensitization of radiotherapy in malignant *** this study,we explored the mechanism underlying curcumin and whether combinin...
详细信息
Activation autophagy contributes to non-apoptotic programmed cell death that facilitates the sensitization of radiotherapy in malignant *** this study,we explored the mechanism underlying curcumin and whether combining curcumin with the inhibition of GLUT-1 has a synergistic effect on the radiosensitivity of laryngeal carcinoma via autophagy by PI3 K/Akt or AMPK *** intensity was detected by transmission electron microscopy,Western blotting,and immunofluorescence..A nude mice xenograft model was established through the injection of Tu212 ***-1 was highly expressed in laryngeal *** reduced radiationmediated GLUT-1 overexpression in laryngeal carcinoma Tu212 *** or GLUT-1 siRNA appeared to improve radiosensitivity by promoting autophagic cell death and cell *** addition,treatment with curcumin or GLUT-1 siRNA or a combination of the two enhanced autophagy status,the key determinant for non-apoptotic cell *** of autophagy using 3-MA promoted cell apoptosis induced by 10 Gy irradiation,curcumin,and GLUT-1 siRNA.3-MA inhibited curcumin and GLUT-1 siRNA-mediated non-apoptotic programmed cell death,which implies that the treatment depends on autophagy *** note,the combination of curcumin,GLUT-1 siRNA,and 3-MA offered the strongest sensitization for laryngeal carcinoma in vivo,suggesting that the inhibition of autophagy further amplified ***,curcumin and the GLUT-1 siRNA-initiated autophagy flux depended on the AMPK-mTOR-ULK1-Beclinl signaling pathway and not the PI3 K-Akt signaling *** treatment primarily caused cell *** combined with curcumin and GLUT-1 siRNA,the improved radiosensitivity of laryngeal carcinoma occurred through not only cell apoptosis but also non-apoptotic cell death,which relies on the autophagy flux activated by the AMPK-mTOR-ULK1-Beclinl pathway.
暂无评论