Background The present study is aimed to explore the role and mechanism of gastric acidified pepsin in promoting laryngeal *** In vitro and in vivo,the effect of acidified pepsin on H+/K+-ATPase,autophagy/mitophagy of...
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Background The present study is aimed to explore the role and mechanism of gastric acidified pepsin in promoting laryngeal *** In vitro and in vivo,the effect of acidified pepsin on H+/K+-ATPase,autophagy/mitophagy of mouse laryngeal epithelial cells was detected by haematoxylin-eosin staining,IHC,CCK8,flow cytometry assays,TUNEL staining,Western Blotting,quantitative real-time PCR,immunofluorescence and transmission electron microscope(TEM).The expression of H+/K+-ATPase α,β-subunits,pepsin in 31 human specimens of normal laryngeal mucosa obtained from laryngocarcinoma patients were analysis by immunohistochemical staining(IHC).results Acidified pepsin(pH3) promoted cell viability and the proportion of S-phase laryngeal epithelial cells in vitro and induced the thickness of mucosa,and cell growth of laryngeal epithelial cells in ***,especially mitophagy,was activated,while mitochondrial membrane potential(MMP) was inhibited after exposure with *** contrast,autophagy inhibited by chloroquine(CQ) abolished acidified pepsin-induced mitophagy and cell viability of laryngeal epithelial *** administration induced cell apoptosis and enlarged the decline of MMP in the presence of pepsin in acidic *** was relationship between H+/K+-ATPase β and α,between H+/K+-ATPase β and pepsin.H+/K+-ATPase knockout or inhibition using pantoprazole further reduced MMP in the presence of acidified pepsin in *** of cell proliferation was mediated by acidified pepsin by upregulating cell apoptosis in vitro and/or in *** In acidic environment,pepsin can upregulate cell viability of laryngeal epithelial cells by activating mitophagy and reducing mitochondria damage via elevating H+/K+-ATPase expression,leading to laryngeal precancerosis.
Background This study is to explore the role of Curcumin and GLUT-1 antisense oligodeoxynucleotides(AS-ODN) on autophagy modulation-initiated *** BALB/c mice was employed to establish xenograft model using Tu212 *** e...
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Background This study is to explore the role of Curcumin and GLUT-1 antisense oligodeoxynucleotides(AS-ODN) on autophagy modulation-initiated *** BALB/c mice was employed to establish xenograft model using Tu212 *** expression of autophagy-and apoptosis-related proteins were determined by *** was observed under transmission electron *** of tumor tissue were detected by TUNEL *** Combinations of Curcumin and GLUT-1 AS-ODN with10 Gy inhibited the tumor growth by inducing apoptosis of laryngeal cancer cells followed with the enhancement of autophagy.3-MA also had a promotion effect on irradiation-mediated growth inhibition possibly by depressing PI3 K and on Curcumin/GLUT-1 AS-ODN-mediated growth inhibition potentially by regulating autophagic *** note,a de-escalation of radiotherapy dose(5 Gy) along with Curcumin,GLUT-1 AS-ODN or 3-MA produced a stronger effect than high dosage of radiotherapy(10 Gy) *** Curcumin and GLUT-1 AS-ODN improve the radiosensitivity of laryngeal carcinoma through regulating autophagy and inducing apoptosis.
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...
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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.
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