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Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma

Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of...

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Detalles Bibliográficos
Autores principales: WEI, SHAO-HUA, LI, WEI, LIU, YANG, GAO, DE-KANG, PAN, JUN, GU, CHUN-WEI, WU, HAO-RONG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919863/
https://www.ncbi.nlm.nih.gov/pubmed/24527069
http://dx.doi.org/10.3892/ol.2013.1773
Descripción
Sumario:Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade.