RP11-874 J12.4 promotes erlotinib resistance in non-small cell lung cancer via increasing AXL expression.
Life Sci
; 351: 122849, 2024 Aug 15.
Article
en En
| MEDLINE
| ID: mdl-38897346
ABSTRACT
EGFR tyrosine kinase inhibitor (TKI) resistance is a major challenge for EGFR-mutant non-small cell lung cancer (NSCLC) treatment. Our previous work revealed that overexpression of AXL promoted EGFR-TKI resistance through epithelial-mesenchymal transition (EMT) in a subset of NSCLC patients. Compared with erlotinib resistant and sensitive cells, RP11-874 J12.4 was upregulated in erlotinib-resistant NSCLC cells (HCC827-ER3). Interestingly, the expression of RP11-874 J12.4 positively correlated with AXL. Besides, RP11-874 J12.4 promotes NSCLC cell proliferation and metastasis in vitro. Mechanistically, RP11-874 J12.4 promoted AXL expression through sponge with miR-34a-5p, which was reported to inhibit the translation of AXL mRNA. Meanwhile, the expression of RP11-874 J12.4 in lung cancer tumors were higher than the adjacent tissue, and those patients with high expression of RP11-874 J12.4 showed a poor prognosis in clinical. High expression of RP11-874 J12.4 might be a biomarker for NSCLC patients with erlotinib resistance. These findings reveal a novel insight into the mechanism of erlotinib resistance in NSCLC, and it might be a promising target for the diagnosis and treatment of NSCLC.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Proteínas Proto-Oncogénicas
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Proteínas Tirosina Quinasas Receptoras
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Carcinoma de Pulmón de Células no Pequeñas
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Resistencia a Antineoplásicos
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Clorhidrato de Erlotinib
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Tirosina Quinasa del Receptor Axl
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Neoplasias Pulmonares
Límite:
Animals
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Humans
Idioma:
En
Revista:
Life Sci
Año:
2024
Tipo del documento:
Article
País de afiliación:
China