Inhibition of δ-catenin palmitoylation slows the progression of prostate cancer.
Biochim Biophys Acta Mol Cell Res
; 1871(5): 119741, 2024 Jun.
Article
en En
| MEDLINE
| ID: mdl-38697304
ABSTRACT
Prostate cancer (PCa) is the second leading cause of death in males. It has been reported that δ-catenin expression is upregulated during the late stage of prostate cancer. Palmitoylation promotes protein transport to the cytomembrane and regulates protein localization and function. However, the effect of δ-catenin palmitoylation on the regulation of cancer remains unknown. In this study, we utilized prostate cancer cells overexpressing mutant δ-catenin (J6A cells) to induce a depalmitoylation phenotype and investigate its effect on prostate cancer. Our results indicated that depalmitoylation of δ-catenin not only reduced its membrane expression but also promoted its degradation in the cytoplasm, resulting in a decrease in the effect of EGFR and E-cadherin signaling. Consequently, depalmitoylation of δ-catenin reduced the proliferation and metastasis of prostate cancer cells. Our findings provide novel insights into potential therapeutic strategies for controlling the progression of prostate cancer through palmitoylation-based targeting of δ-catenin.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias de la Próstata
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Cadherinas
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Progresión de la Enfermedad
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Proliferación Celular
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Cateninas
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Lipoilación
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Catenina delta
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Biochim Biophys Acta Mol Cell Res
Año:
2024
Tipo del documento:
Article
País de afiliación:
China