RESUMEN
<p><b>OBJECTIVE</b>To study the relationship of changes in gene expression profiles of hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts.</p><p><b>METHODS</b>The differentially expressed genes were analyzed in two pairs of tissues of hydatidiform mole versus normal villi, and in two pairs of normal primary culture trophoblasts versus JAR cell line of chariocarcinoma, using cDNA microarray containing 4096 genes. To confirm the results of cDNA microarray analysis, expressions of some up-regulated genes related to DNA synthesis in normal villi, hydatidiform mole, and 2 choriocarcinoma cell lines (JAR and JEG-3) were examined by immunohistochemistry, immunoblotting and RT-PCR.</p><p><b>RESULTS</b>A total of 89 genes were differentially expressed in all hydatidiform moles, accounting for 2.2% of the genes arrayed. Of the 89 genes, 24 were up-regulated and 65 were down-regulated. Compared with normal primary trophoblasts, there were 433 genes up-regulated and 380 genes down-regulated in JAR cell line. Forty six genes were up-regulated in both hydatidiform mole and choriocarcinoma, while 13 genes were down-regulated. Some genes associated with cell proliferative inhibition were significantly down-regulated, whereas those associated with cell proliferation, malignant transformation, metastasis and drug resistance were highly up-regulated. The expressions of thymidine kinase 1, the small subunit of ribonucleotide reductase (RRM2) were significantly increased in hydatidiform mole, JAR and JEG-3 cells.</p><p><b>CONCLUSION</b>Abnormal expression of genes exists in hydatidiform mole and choriocarcinoma. Hyperplasia of trophoblasts may be related to over-expression of genes coding for synthetic enzymes.</p>
Asunto(s)
Adulto , Femenino , Humanos , Embarazo , Línea Celular Tumoral , Proliferación Celular , Transformación Celular Neoplásica , Coriocarcinoma , Genética , Metabolismo , Patología , Resistencia a Antineoplásicos , Perfilación de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Mola Hidatiforme , Genética , Metabolismo , Hiperplasia , Metástasis de la Neoplasia , Análisis de Secuencia por Matrices de Oligonucleótidos , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Ribonucleósido Difosfato Reductasa , Metabolismo , Timidina Quinasa , Metabolismo , Trofoblastos , Patología , Neoplasias Uterinas , Genética , Metabolismo , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To evaluate the inhibitory effect of tumor suppressor PTEN on cell growth of endometrial carcinoma.</p><p><b>METHODS</b>The exogenous wild PTEN cDNA via an adenoviral vector (Ad-PTEN) was introduced into Ishikawa cells. The expression of PTEN protein was detected by Western blot. The growth of Ishikawa cells was evaluated by trypan blue exclusion method and MTT.</p><p><b>RESULTS</b>The expression of PTEN protein was induced on day 1, and greatly increasing on day 3 - 5 after Ad-PTEN infection. The expression of PTEN significantly inhibited the growth of Ishikawa cells, and also significantly inhibited the growth of Ishikawa cells induced by IGF-II.</p><p><b>CONCLUSION</b>Adenovirus-mediated introduction of exogenous PTEN into human endometrial carcinoma cells can induce growth suppression. PTEN gene may be a novel therapeutic agent for endometrial carcinoma.</p>
Asunto(s)
Femenino , Humanos , Adenoviridae , Genética , Proliferación Celular , Neoplasias Endometriales , Metabolismo , Patología , Regulación Neoplásica de la Expresión Génica , Factor II del Crecimiento Similar a la Insulina , Farmacología , Fosfohidrolasa PTEN , Monoéster Fosfórico Hidrolasas , Genética , Fisiología , Recombinación Genética , Transfección , Proteínas Supresoras de Tumor , Genética , FisiologíaRESUMEN
<p><b>OBJECTIVE</b>To determine candidate genes of endometrial adenocarcinoma.</p><p><b>METHODS</b>To compare the gene expression profile in 2 endometrial adenocarcinoma tissues and 2 normal endometria by HGEC-40s GeneChip probe including 4096 genes array. Expression differences between normal and malignant tissue groups were measured by GenePixPro3.0 software.</p><p><b>RESULTS</b>350 genes with a ratio below 0.5 and above 2.0 showed discrimination between normal and malignant groups. Thirty three genes with ratio above 3 were up-regulated, forty-four genes with ratio below 0.3 were down-regulated.</p><p><b>CONCLUSION</b>The overexpression of oncogenes with their disturbed or constitutively activated signal transduction cascades alone or in combination with the mutation-induced silencing of tumor suppressor genes is associated with malignant transformation.</p>