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1.
Biomedical and Environmental Sciences ; (12): 332-338, 2008.
Artigo em Inglês | WPRIM | ID: wpr-296042

RESUMO

<p><b>OBJECTIVE</b>To analyze the relationship between malignant transformation and abnormal expression of eukaryotic initiation factor 3 (eIF3 p36) in human bronchial epithelial (16HBE) cells induced by cadmium chloride (CdCl2).</p><p><b>METHODS</b>16HBE cells were treated several times with different concentrations of CdCl2. Tumorigenic potential of transformed cells was identified by assays for anchorage-independent growth in soft agar and for tumorigenicity in nude mice after the 35th passage. Total RNA was isolated from 16HBE cells induced by CdCl2, including non-transformed, Cd-transformed, and Cd-tumorigenic cell lines. Special primers for eIF3 p36 were designed and the expression of eIF3 mRNA in different cell lines was detected with fluorescent quantitative-polymerase chain reaction technique (FQ-PCR).</p><p><b>RESULTS</b>The 35th passage of 16HBE cells transformed by CdCl2 exhibited overlapping growth. Compared with the non-transformed cells, colonies of transformed cell lines in soft agar showed statistically significant increases and dose-dependent effects (P<0.01). All Cd-induced transformed cell lines formed tumors in nude mice within 2 weeks of inoculation, but none of the mice injected with non-transformed cells showed tumors even after 3 weeks. All tumors were pathologically identified as poorly differentiated squamous cell carcinoma. The eIF3 p36 genes in different stages of 16HBE cells transformed by CdCl2 were elevated as compared with the non-transformed control (P<0.01), and the eIF3 expression increased with the degree of cell malignancy.</p><p><b>CONCLUSION</b>CdCl2 is capable of inducing morphological transformation in 16HBE cells and transformed cells are potentially tumorigenic. Over-expression of eIF3 p36 is positively correlated with malignant transformation of 16HBE cells induced by CdCl2 and may be one of the molecular mechanisms potentially responsible for carcinogenesis due to Cd.</p>


Assuntos
Animais , Humanos , Camundongos , Sequência de Bases , Brônquios , Biologia Celular , Metabolismo , Cloreto de Cádmio , Farmacologia , Transformação Celular Neoplásica , Primers do DNA , Células Epiteliais , Metabolismo , Fatores de Iniciação em Eucariotos , Metabolismo , Camundongos Nus , Reação em Cadeia da Polimerase
2.
Biomedical and Environmental Sciences ; (12): 53-60, 2006.
Artigo em Inglês | WPRIM | ID: wpr-229725

RESUMO

<p><b>OBJECTIVE</b>To study the oncogenic potential of mouse translation initiation factor 3 (TIF3) and elongation factor-1delta (TEF-1delta) in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide (NiS).</p><p><b>METHODS</b>Abnormal expressions of human TIF3 and TEF-1delta genes in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were investigated and analyzed by the reverse transcript polymerase chain reaction (RT-PCR) and fluorescent quantitative polymerase chain reaction (FQ-PCR), respectively.</p><p><b>RESULTS</b>RT-PCR analysis primarily showed that both human TIF3 and TEF-1delta mRNA expressions in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were increased as compared with controls. FQ-PCR assay showed that the levels of TIF3 expressions in the transformed cells and tumorigenic cells were 3 and 4 times higher respectively, and the elevated expressions of TEF-1delta cDNA copies were 2.7- to 3.5-fold in transformed cells and 4.1- to 5.2-fold in tumorigenic cells when compared with non-transformed cells, indicating that the over-expressions of human TIF3 and TEF-1delta genes were related to malignant degree of the cells induced by nickel.</p><p><b>CONCLUSIONS</b>These findings demonstrate that there are markedly abnormal expressions of TIF3 and TEF-1delta genes during malignant transformation of human bronchial epithelial cell lines induced by crystalline NiS. They seem to be the molecular mechanisms potentially responsible for human carcinogensis due to nickel.</p>


Assuntos
Humanos , Biomarcadores , Brônquios , Biologia Celular , Linhagem Celular Transformada , Linhagem Celular Tumoral , Transformação Celular Neoplásica , Metabolismo , DNA Complementar , Metabolismo , Células Epiteliais , Regulação Neoplásica da Expressão Gênica , Níquel , Toxicidade , Fator 1 de Elongação de Peptídeos , Genética , Metabolismo , Fator de Iniciação 3 em Procariotos , Genética , Metabolismo
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