Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective is to eliminate the interference from other cell types; gene fragments involved in endometrial carcinoma (EC) are screened and cloned. Human normal endometrial glandular epithelia and EC cells were harvested with laser capture microdissection (LCM). The purification and concentration of minimal RNA were used to screen differential expressed gene fragments involved in EC by fluoro differential display polymerase chain reaction (FDD-PCR). The differential gene fragments were cloned, sequenced, and then identified by reverse Northern blot hybridization. Positive fragments were analyzed with basic local alignment search tool (BLAST). Cyclin-dependent kinase 7 (CDK7) expressions in EC and normal endometrial tissue were tested by immunohistochemical staining. Of 38 differential bands, 3 bands were of high expression in normal endometrium and 35 in EC. Six positive differential gene fragments were obtained and BLAST analysis for them suggested that L1.1 was homologous (99% identical) to the CDK7; L1.9 had a 99% homology with protein phosphatase 1 regulatory (inhibitor) subunit 12 A (PPP1R12A); L1.21 and L1.22 showed a 100% homology with cellular repressor of E1A-stimulated genes 1 (CREG); and L1.25 and L1.26 indicated more than 98% homology with solute carrier family 39 (zinc transporter), member 10 (SLC39A10). Immunohistochemistry revealed that CDK7 expression was higher in EC than in normal endometrium. We conclude that pathogenic genes involved in EC are obtained with LCM and FDD-PCR. It has been first found that CDK7, PPP1R12A, CREG, and SLC39A10 are correlative with EC from gene level. CDK7 is strongly associated with EC and can be used as potential molecular marker of EC for further studies.
 ...
PMID:Application of laser capture microdissection and differential display technique for screening of pathogenic genes involved in endometrial carcinoma. 1745 60

Lipolysis-stimulated lipoprotein receptors (LSRs) localize to tricellular tight junctions. Recent studies have shown that changes in the localization and expression profiles of LSRs are associated with malignancy of endometrial carcinomas, although the precise mechanisms by which malignant progression induces changes in the localization of LSRs are still unknown. In this study, we found that changes in cell tension correlated with alterations in the junctional localization of LSRs in endometrial cancer Sawano cells. At high cell densities, myosin phosphatase target subunit 1 (MYPT1) localized to bicellular junctions, whereas activated myosin regulatory light chain 2 (MRLC2) was dislocated from these regions, suggesting that circumferential tensile forces decreased at high cell densities. Under these conditions, LSRs localized to tricellular junctions. In contrast, a phosphorylated form of MRLC2 localized to bicellular regions, while MYPT1 was excluded from these regions, suggesting that tensile forces formed along the circumferential edge at low cell densities. It is noteworthy that, when cells were cultured under these conditions, LSRs localized to bicellular regions. Upon treatment with a myosin inhibitor, LSR localization in bicellular junctions decreased at low cell densities. Overall, our results indicate that the modulation of cellular tension was involved in the translocation of LSRs from bicellular to tricellular tight junctions.
 ...
PMID:The bicellular tensile force sorts the localization of LSRs in bicellular and tricellular junctions. 2849 78