LncRNA HOTAIR contributes Taxol-resistance of hepatocellular carcinoma cells via activating AKT phosphorylation by down-regulating miR-34a.
Biosci Rep
; 40(7)2020 07 31.
Article
em En
| MEDLINE
| ID: mdl-32700738
ABSTRACT
Drug resistance of Taxol leads to the treatment failure in hepatocellular carcinoma (HCC). LncRNA HOTAIR have drawn increasing attention in various diseases; its function and mechanism in Taxol-resistance in HCC remain unclear. In the present study, the two Taxol resistant HCC cell lines (HepG2/Taxol and SMMC7721/Taxol) were induced. The qRT-PCR data exhibited that over-expressed HOTAIR as well as low-expressed miR-34a were founded in HepG2/Taxol and SMMC7721/Taxol cells. HOTAIR knockdown suppresses proliferation, invasion and promotes apoptosis of in HepG2/Taxol and SMMC7721/Taxol cells through up-regulating miR-34a by MTT assay, transwell invasion assays and flow cytometry, while down-regulation of miR-34a had an opposite effect on reversing Taxol resistance. Cleaved caspase-3 and Bax were significantly up-regulated by si-HOTAIR transfection, while Bcl-2 level exhibited opposite trend. Besides, HOTAIR knockdown impaired Taxol-resistance in HCC by accommodating Akt phosphorylation and Wnt/ß-catenin signaling via interacting with miR-34a. The present study may afford a valuable target for treating Taxol-resistance in HCC.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Temas:
Geral
/
Tipos_de_cancer
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Outros_tipos
Base de dados:
MEDLINE
Assunto principal:
Paclitaxel
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Carcinoma Hepatocelular
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Resistencia a Medicamentos Antineoplásicos
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MicroRNAs
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RNA Longo não Codificante
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Neoplasias Hepáticas
Limite:
Humans
Idioma:
En
Revista:
Biosci Rep
Ano de publicação:
2020
Tipo de documento:
Article
País de afiliação:
China