ANXA2 could act as a moderator of EGFR-directed therapy resistance in triple negative breast cancer.
Biosci Biotechnol Biochem
; 82(10): 1733-1741, 2018 Oct.
Article
en En
| MEDLINE
| ID: mdl-29912633
ABSTRACT
Triple negative breast cancer (TNBC) patients cannot benefit from EGFR-targeted therapy even though the EGFR is highly expressed, because patients exhibit resistance to these drugs. Unfortunately, the molecular mechanisms remain relatively unknown. ANXA2, highly expressed in invasive breast cancer cells, is closely related with poor prognosis, and acts as a molecular switch to EGFR activation. In this study, MDA-MB-231 cells and MCF7 cells were used. Our results showed that ANXA2 expression is inversely correlated with cell sensitivity to gefitinib. Knockdown of ANXA2 expression in MDA-MB-231 cells increased the gefitinib induced cell death. When ANXA2 was overexpressed in MCF7 cells, the gefitinib induced cell death was decreased. Furthermore, we demonstrated that phosphorylation of ANXA2 at Tyr23 is negatively correlated with the sensitivity of TNBC to gefitinib. Altogether, our results suggest a new role of ANXA2 in regulating sensitivity of TNBC MDA-MB-231 cells to the EGFR inhibitor gefitinib.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Anexina A2
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Resistencia a Antineoplásicos
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Inhibidores de Proteínas Quinasas
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Neoplasias de la Mama Triple Negativas
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Receptores ErbB
Tipo de estudio:
Prognostic_studies
Límite:
Female
/
Humans
Idioma:
En
Revista:
Biosci Biotechnol Biochem
Asunto de la revista:
BIOQUIMICA
/
BIOTECNOLOGIA
Año:
2018
Tipo del documento:
Article
País de afiliación:
China