RESUMEN
<p><b>BACKGROUND</b>Small cell lung cancer (SCLC) is the most aggressive form of lung cancer. This study aimed to investigate the mechanism of human small cell lung cancer cell line resistance to etoposide (VP-16), H446/VP.</p><p><b>METHODS</b>The cell viability was measured by MTT assay. Immunocytochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting methods were used to detect the multidrug resistance gene (MDR1), bcl-2, bax and the topoisomerase II (Topo II) expressions in H446 and H446/VP cells after treated with or without VP-16.</p><p><b>RESULTS</b>The 50% inhibition concentration (IC50) of VP-16 on H446 cells was 49 mg/L, and 836 mg/L was for H446/VP cells. The expressions of MDR1 and bcl-2 were up-regulated, while the amounts of bax and Topo II were reduced in H446/VP cells. After treated with 49 mg/L of VP-16, it showed that the drug could significantly inhibit bcl-2 and Topo II expressions, and increase bax expression in H446 cells compared with that of H446/VP cells.</p><p><b>CONCLUSIONS</b>The H446/VP cell was stably resistant to VP-16. The decreased expression of Topo II was correlated with the H446/VP multidrug resistance. The elevated expressions of MDR1, and the altered apoptotic pathways also played an important role in VP-16 induced multidrug resistance of SCLC.</p>
Asunto(s)
Humanos , Subfamilia B de Transportador de Casetes de Unión a ATP , Miembro 1 de la Subfamilia B de Casetes de Unión a ATP , Genética , Metabolismo , Antígenos de Neoplasias , Genética , Metabolismo , Western Blotting , Línea Celular Tumoral , ADN-Topoisomerasas de Tipo II , Genética , Metabolismo , Proteínas de Unión al ADN , Genética , Metabolismo , Resistencia a Múltiples Medicamentos , Genética , Fisiología , Resistencia a Antineoplásicos , Genética , Fisiología , Inmunohistoquímica , Proteínas Proto-Oncogénicas c-bcl-2 , Genética , Metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Carcinoma Pulmonar de Células Pequeñas , MetabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of IL-24 expression on the growth of glioma cells.</p><p><b>METHODS</b>The IL-24 gene was transfected into rat glioma C6 cells with a retroviral vector. The expression of IL-24 in C6/IL-24 glioma cells was confirmed by RT-PCR. MTT assay and flow cytometry were used to study tumor cell proliferation in vitro. Tumorigenicity in vivo was studied in inbred SD male rats by the growth of intracerebrally inoculated tumor.</p><p><b>RESULTS</b>It was confirmed by RT-PCR that the exogenous IL-24 gene expressed in C6/IL-24 cell. The C6/IL-24 cell proliferation in vitro and tumorigenicity in vivo were both inhibited compared with its parental C6 cell.</p><p><b>CONCLUSION</b>IL-24 expression in glioma cells somehow inhibits their growth in vitro and in vivo.</p>