Study Of Gene Expression Profile And Mechanism Of Invasion And Metastasis In Endometrioid Endometrial Carcinoma

Part OneGene Expression Profile in Endometrioid Endometrial Carcinoma Objective Recent investigations of the carcinogenesis shows that it is a multiple-step cell cycle process with participation of many causative factors and genes. The traditional tumor investigation technology can no longer meet the demand of research work due to the complicated procedures, low automatism, few manipulating array and low laboratory efficacies. The incidence of endometrial carcinoma increases rapidly year by year and tends to occur more in younger-aged groups. Thus, it is very important to investigate the mechanism of carcinogenesis, enabling early prevention and detection. This study reports our works on the gene expression profile with the application of high flux gene chip probe technology and with the aim to find out the candidate genes of endometrioid endometrial carcinoma.Methods Expression of 4096 genes was quantified in 2 malignant and 2 normal endometrial specimens using HGEC-40s Gene-Chip Probe Array. Expression differences between normal and malignant tissue groups were measured by GenePixPro3.0 software.Results Three hundred and fifty genes with a ratio below 0.5 and above 2.0 provided discrimination between normal and malignant groups. Sixty-eight genes with ratio above 2.5 were up-regulated, 44 genes with ratio below 0.3were down-regulated. Bio-informatics analysis of the down-regulated 44 genes with significant differences were as follows: (1) primary oncogene and tumor suppressor gene 2, (2) cell cycle protein 4, (3) cytoskeleton and movement 6, (4) DNA synthesis, repair and recombinant protein 2, (5) DNA conjugation, transcription and transcriptional factor 2, (6) cell receptor 2, (7) immunologic associated 2, (8) cell signaling and transport protein 9, (9) metabolism 4, (10) development associated 2, (11) others 9. Bio-informatics analysis of the up-regulated 68 genes with significant difference in expression were as follows: (1) primary oncogene and tumor suppressor gene 1 stripe, (2) ionic pathway and transport protein 3, (3) cell cycle protein 3, (4) cytoskeleton and movement 3, (5) immunologic associataed 2, (6) cell signal and transport protein 14, (7) metabolism 18, (8) protein translocation synthesis 4, (9) development associated 3, (10) others 14, ( 11 ) DNA conjugation, transcription and transcriptional factor 1 , (12) cell receptor 2Conclusion This study shows that the over-expression 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. The simultaneous hybridization of labeled cDNA to an array of oligonucleotides representative for several thousand genes permits the identification and quantification of expressed genes and will help to find out the candidate genes, hence we can have a reasonably effective strategy of preventing and treating endometrioid endometrial carcinoma.