The Effect of IkappaBalpha-SR Gene Transfer on the Sensitivity of Human Lung Cancer Cell Lines to Cisplation and Paclitaxel / 결핵
Tuberculosis and Respiratory Diseases
;
: 122-134, 2001.
Artigo
em Coreano
| WPRIM
| ID: wpr-36115
ABSTRACT
BACKGROUND:
Some chemotherapeutic drugs induce NF-κB activation by degrading the IκBα protein in cancer cells which contributes to anticancer drug resistance. We hypothesized that inhibiting IκBα degradation would block NF-κB activation and result in increased tumor cell mortality in response to chemotherapy.METHODS:
The "superrepressor" form of the NF-κB inhibitor was transferred by an adenoviral vector (Ad-IκBα-SR) to the human lung cancer cell lines (NCI H157 and NCI H460). With a MTT assay, the level of sensitization to cisplatin and paclitaxel were measured. To confirm the mechanism, an EMSA and Annexin V assay were performed.RESULTS:
EMSA showed that IκBα-SR effectively blocked the NF-κB activation induced by cisplatin. Transduction with Ad-IκBα-SR resulted in an increased sensitivity of the lung cancer cell lines to cisplatin and paclitaxel by a factor of 2~3 in terms of IC50. Annexin-V analysis suggests that this increment in chemosensitivity to cisplatin probably occurs through the induction of apoptosis.CONCLUSION:
The blockade of chemotherapeutics induced NF-κB activation by inducing Ad-IκBα-SR, increased apoptosis and increasing the chemosensitivity of the lung cancer cell lines tested, subsequently. Gene transfer of IκBα-SR appears to be a new therapeutic strategy of chemosensitization in lung cancer.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Resistência a Medicamentos
/
Linhagem Celular
/
Adenoviridae
/
Mortalidade
/
Cisplatino
/
Paclitaxel
/
Apoptose
/
Anexina A5
/
Concentração Inibidora 50
/
Tratamento Farmacológico
Tipo de estudo:
Estudo diagnóstico
/
Estudo prognóstico
Limite:
Humanos
Idioma:
Coreano
Revista:
Tuberculosis and Respiratory Diseases
Ano de publicação:
2001
Tipo de documento:
Artigo
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