Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Endometrial cancer develops as a result of abnormal cell growth associated with uncontrolled cell proliferation, excessive activation of signaling pathways and miRNA activity. The aim of this study was to determine the expression profile of genes associated with cell proliferation and to assess which miRNAs can participate in the regulation of their expression. The study enrolled 40 patients with endometrial cancer and 10 patients without neoplastic changes. The expression profile of genes associated with cell proliferation and the expression profile of miRNAs were assessed using microarrays. RT-qPCR was performed to validate mRNA microarray results. The mirTAR tool was used to identify miRNAs that regulate the activity of genes associated with cell proliferation. Decreased expression of and , as well as overexpression, were observed in endometrial cancer using both mRNA microarrays and RT-qPCR. Microarray analysis showed low levels of and , but this was only partially validated using RT-qPCR. Reduced activity of may be caused by increased miR-200c, miR-155 and miR-200b expression. Cell proliferation is disturbed in endometrial cancer, which may be associated with an overexpression of miR-200a, miR-200c, and miR-155, making it a potential diagnostic marker.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928856PMC
http://dx.doi.org/10.3390/ijms20236011DOI Listing

Publication Analysis

Top Keywords

cell proliferation
24
endometrial cancer
20
genes associated
16
associated cell
16
expression profile
12
profile genes
8
microarrays rt-qpcr
8
mir-200c mir-155
8
cell
7
associated
6

Similar Publications

Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.

View Article and Find Full Text PDF

X-Linked Hypophosphatemia: Role of Fibroblast Growth Factor 23 on Human Skeletal Muscle-Derived Cells.

Calcif Tissue Int

September 2025

FirmoLab, Fondazione F.I.R.M.O. Onlus and Stabilimento Chimico Farmaceutico Militare (SCFM), 50141, Florence, Italy.

X-linked hypophosphatemia (XLH) is a rare and progressive disease, due to inactivating mutations in the phosphate-regulating endopeptidase homolog X-linked (PHEX) gene. These pathogenic variants result in elevated circulating levels of fibroblast growth factor 23 (FGF23), responsible for the main clinical manifestations of XLH, such as hypophosphatemia, skeletal deformities, and mineralization defects. However, XLH also involves muscular disorders (muscle weakness, pain, reduced muscle density, peak strength, and power).

View Article and Find Full Text PDF

Integrins from extracellular vesicles as players in tumor microenvironment and metastasis.

Cancer Metastasis Rev

September 2025

Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-Sur-Yvette, 91198, France.

Integrins constitute a large and diverse family of cell adhesion molecules that play essential roles in regulating tumor cell differentiation, migration, proliferation, and neovascularization. Tumor cell-derived exosomes, a subtype of extracellular vesicles, are enriched with integrins that reflect their cells of origin. These exosomal integrins can promote extracellular matrix remodeling, immune suppression, and vascular remodeling and are closely linked to tumor progression and metastasis, acting as pivotal players in mediating organ-specific metastasis.

View Article and Find Full Text PDF

Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by ubiquitous deficiency in the SMN protein. The identification of disease modifiers is key to understanding pathogenic mechanisms and broadening the range of targets for developing SMA therapies that complement SMN upregulation. Here, we report a cell-based screen that identified inhibitors of p38 mitogen-activated protein kinase (p38 MAPK) as suppressors of proliferation defects induced by SMN deficiency in mouse fibroblasts.

View Article and Find Full Text PDF

In recent years, there has been a rapid increase in the incidence of thyroid carcinoma (TC). Our study focuses on the regulatory effect of circular RNAs on metabolism of TC, aiming to provide new insights into the mechanisms of progression and a potential therapeutic target for TC. In this study, we identified high expression levels of circPSD3 in TC tissues through RNA sequencing.

View Article and Find Full Text PDF