Publications by authors named "I Jaitovich Groisman"
Article Synopsis
- Prostate cancer is highly lethal, and the expression levels of miR-145-5p, a potential molecular marker, are often low in tumors, though its functions are not well understood.
- Bioinformatics and various experimental techniques identified lnc-ZNF30-3 as a potential competing endogenous RNA that sponges miR-145-5p and is upregulated in prostate cancer, correlating with worse patient outcomes.
- The study demonstrates that lnc-ZNF30-3 influences cancer cell migration and EMT markers, indicating its role in prostate cancer progression and highlighting its potential as a therapeutic target.
TWIST1 is a basic helix-loop-helix transcription factor, and one of the master Epithelial-to-Mesenchymal Transition (EMT) regulators. We show that tumor suppressor miR-145-5p controls TWIST1 expression in an immortalized prostate epithelial cell line and in a tumorigenic prostate cancer-derived cell line. Indeed, shRNA-mediated miR-145-5p silencing enhanced TWIST1 expression and induced EMT-associated malignant properties in these cells.
View Article and Find Full Text PDFThe cytoplasmic element binding protein 1 (CPEB1) regulates many important biological processes ranging from cell cycle control to learning and memory formation, by controlling mRNA translation efficiency via 3' untranslated regions (3'UTR). In the present study, we show that CPEB1 is significantly downregulated in human Glioblastoma Multiforme (GBM) tissues and that the restoration of its expression impairs glioma cell lines growth. We demonstrate that CPEB1 promotes the expression of the cell cycle inhibitor p27(Kip1) by specifically targeting its 3'UTR, and competes with miR-221/222 binding at an overlapping site in the 3'UTR, thus impairing miR-221/222 inhibitory activity.
View Article and Find Full Text PDFArticle Synopsis
- The roles of miRNAs and other regulatory proteins, specifically CPEB1, in controlling mRNA expression at the 3'UTR remain unclear.
- Research indicates that CPEB1 and miR-15b both repress WEE1, a critical cell cycle regulator, during G1 and S phases but switch to promoting WEE1 translation during the G2/M transition, highlighting the dynamic nature of translational control in cell cycle regulation.
Background: We sought to determine whether the response of pulmonary elimination of CO2 (VCO2) to a sudden increase in positive end-expiratory pressure (PEEP) could predict fluid responsiveness and serve as a noninvasive surrogate for cardiac index (CI).
Methods: Fifty-two patients undergoing cardiovascular surgery were included in this study. By using a constant-flow ventilation mode, we performed a PEEP challenge of 1-minute increase in PEEP from 5 to 10 cm H2O.