GOLPH3 inhibits erastin-induced ferroptosis in colorectal cancer cells.
Cell Biol Int
; 48(8): 1198-1211, 2024 Aug.
Article
em En
| MEDLINE
| ID: mdl-38825780
ABSTRACT
Ferroptosis is a novel form of programmed cell death and is considered to be a druggable target for colorectal cancer (CRC) therapy. However, the role of ferroptosis in CRC and its underlying mechanism are not fully understood. In the present study we found that a protein enriched in the Golgi apparatus, Golgi phosphoprotein 3 (GOLPH3), was overexpressed in human CRC tissue and in several CRC cell lines. The expression of GOLPH3 was significantly correlated with the expression of ferroptosis-related genes in CRC. The overexpression of GOLPH3 in Erastin-induced Caco-2 CRC cells reduced ferroptotic phenotypes, whereas the knockdown of GOLPH3 potentiated ferroptosis in HT-29 CRC cells. GOLPH3 induced the expression of prohibitin-1 (PHB1) and prohibitin-2 (PHB2), which also inhibited ferroptosis in Erastin-treated CRC cells. Moreover, GOLPH3 interacted with PHB2 and nuclear factor erythroid 2-related factor 2 (NRF2) in Caco-2 cells. These observations indicate that GOLPH3 is a negative regulator of ferroptosis in CRC cells. GOLPH3 protects these cells from ferroptosis by inducing the expression of PHB1 and PHB2, and by interacting with PHB2 and NRF2.
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Base de dados:
MEDLINE
Assunto principal:
Piperazinas
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Proteínas Repressoras
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Neoplasias Colorretais
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Ferroptose
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Proibitinas
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Proteínas de Membrana
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article