Background & Objective: PTEN is a tumor suppressor gene with phosphatase activity. It had been proved the aberrant expression and mutation of PTEN in diverse types of human cancer; PTEN is closely associated with occurrence and development of malignant tumor. This study was conducted to investigate the expression of PTEN/MMAC1/TEP1 gene product in human renal cell carcinoma (RCC) and the correlation between the expression of PTEN and the biological behaviors of RCC.
Methods: The PTEN protein of 44 cases of RCC tissues confirmed by pathology after operation, 15 cases of adjacent normal renal tissues, and 10 cases of non-tumor normal renal tissues were assessed using immunohistochemical technique (SP). Fifteen RCC tissues and 10 normal renal tissues selected respectively from the renal tissues whose PTEN protein expression were positive as well as those from the negative were made to be the cell suspension mingled with paraffin. The proliferative index and the apoptosis incidence were examined by flow cytometry and the correlation between PTEN protein and the proliferation and apoptosis were analyzed.
Results: The expression of PTEN protein was mostly located in the renal cell plasma. The positive incidence of expression PTEN protein in RCC was 36.3% which was prominently lower than those in the adjacent normal tissues (77.3%) and the normal tissues (100.00%) (P< 0.01). There was no significant difference between the different sorts of tissues (P >0.05). The expression of PTEN in stage I, II is much higher than that in stage III, IV(P< 0.05). The proliferative index of RCC whose expression of PTEN protein was positive (5.6+/-0.8)% was significantly lower than that of negative (15.6+/-1.6)% (P< 0.01). While the apoptosis incidence was (6.5+/-1.9)%,which was much higher than that of RCC whose expression was (2.9+/-1.6)% (P< 0.01).
Conclusion: The positive expression incidence of PTEN protein significantly decreases in RCC tissues. PTEN protein suppresses carcinoma by inducing the cell cycle to be blocked up in G1 phase and increasing the apoptosis incidence. The assessment of the expression PTEN protein is one of the important indexes of the development and prognosis of RCC.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Impact of 17-alpha ethinyl estradiol (EE2) and diethyl phthalate (DEP) exposure on microRNAs expression and their target genes in differentiated SH-SY5Y cells.
Sci Rep
January 2025
Department of Pharmacy and BioTechnology - FaBiT, Alma Mater Studiorum - University of Bologna, via Irnerio 48, Bologna, 40126, Italy.
Environmental endocrine disruptor chemicals (EDCs) have raised significant concerns due to their potential adverse effects on human health, particularly on the central nervous system (CNS). This study provides a comparative analysis of the effects of 17-alpha ethinyl estradiol (EE2) and diethyl phthalate (DEP) on neuronal cell proliferation and neurotoxicity. Using differentiated SH-SY5Y human neuronal cells, we evaluated cell viability, microRNA (miRNA) regulation, and RNA expression following exposure to subtoxic concentrations of EE2 and DEP.
View Article and Find Full Text PDFFeedback loop centered on MAF1 reduces blood-brain barrier damage in sepsis-associated encephalopathy.
Cell Mol Biol Lett
January 2025
Department of Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Background: A previous study found that MAF1 homolog, a negative regulator of RNA polymerase III (MAF1), protects the blood-brain barrier (BBB) in sepsis-associated encephalopathy (SAE); however, the related molecular mechanisms remain unclear.
Subjects And Methods: In this study, a rat sepsis model was constructed using the cecum ligation and puncture (CLP) method. In vitro, rat brain microvascular endothelial cells and astrocytes were stimulated with serum from the sepsis model rats.
Regarding flotillin knockdown, drug resistance is reversed in colorectal cancer (CRC) cell lines; this is associated with the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway, as our previous experimental results indicated. However, the exact mechanism underlying this pathway remains unclear. PI3K inhibitor and activator were added separately to clarify the role of the PI3K pathway in reversing drug resistance.
View Article and Find Full Text PDFApigenin enhancing oxidative resistance and proteostasis to extend lifespan via PTEN-mediated AKT signalling pathway.
Biochim Biophys Acta Mol Basis Dis
January 2025
State Key Laboratory of Subtropical Silviculture, Zhejiang A & F University, Hangzhou 311300, China; Department of Pharmaceutical Botany, School of Pharmacy, Naval Medical University, Shanghai 200433, China. Electronic address:
Aging is a complicated process, featuring the progressive deterioration of physiological functions and a heightened susceptibility to diseases including neurodegenerative disorders, cardiovascular diseases, and cancer. Apigenin, a flavonoid existing in various plants, has attracted attention due to its potential role in anti-aging. In this investigation, the potential effect of apigenin on extending lifespan in Saccharomyces cerevisiae (yeast) and Drosophila melanogaster (flies) was explored.
View Article and Find Full Text PDFMale sex determination maintains proteostasis and extends lifespan of daf-18/PTEN deficient C. elegans.
EMBO Rep
January 2025
The Zhongzhou Laboratory for Integrative Biology, Henan University, 450000, Zhengzhou, Henan, China.
Although females typically have a survival advantage, those with PTEN functional abnormalities face a higher risk of developing tumors than males. However, the differences in how each sex responds to PTEN dysfunction have rarely been studied. We use Caenorhabditis elegans to investigate how male and hermaphrodite worms respond to dysfunction of the PTEN homolog daf-18.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!