Aloe gel glucomannan induced colon cancer cell death via mitochondrial damage-driven PINK1/Parkin mitophagy pathway.
Carbohydr Polym
; 295: 119841, 2022 Nov 01.
Article
en En
| MEDLINE
| ID: mdl-35989033
Mitophagy can selectively remove damaged mitochondria, which is critical in regulating mitochondrial homeostasis in diseases, such as cancer. Herein, we found that Aloe gel glucomannan (AGP) significantly inhibited the proliferation of colon cancer cells. RNA-seq analysis revealed that AGP upregulated autophagy, lysosome and mitochondrial fission signal pathways in colon cancer cell line CT26. Notably, AGP induced the accumulation of impaired and reactive oxygen species (ROS)-generating mitochondria, which triggered excessive mitophagy. Interestingly, the mitophagy activator enhanced AGP-induced mitophagy and cytotoxicity, whereas the mitophagy inhibitor reversed the influence of AGP. Furthermore, activation of PINK1/Parkin mitophagy pathway and transcription factor EB (TFEB) signaling was dependent on ROS overproduction. Taken together, these results indicated that AGP induced cytotoxic mitophagy through ROS-related PINK1/Parkin pathway and TFEB activation in CT26 cells. The research would provide theoretical basis for the development of AGP as a promising anticancer agent.
Palabras clave
Aloe gel glucomannan; Ammonium sulfate (PubChem CID: 6097028); Crystal Violet (PubChem CID: 11057); DAPI (PubChem CID: 2954); Ethanol (PubChem CID: 702); FCCP (PubChem CID: 3330); Hoechst 33342 (PubChem CID: 1464); Mdivi-1 (PubChem CID: 3825829); MitoTracker Red (PubChem CID: 22613925); Mitophagy; N-Acetyl-L-cysteine (PubChem CID: 12035); Phenol (PubChem CID: 996); ROS; Rapamycin (PubChem CID: 5284616); Sulfuric Acid (PubChem CID: 1118); TFEB; Triton X-100 (PubChem CID: 5590); colon cancer
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas Quinasas
/
Neoplasias del Colon
/
Ubiquitina-Proteína Ligasas
/
Aloe
/
Antineoplásicos
Límite:
Humans
Idioma:
En
Revista:
Carbohydr Polym
Año:
2022
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido