Phosphatase and Tensin Homologue: Novel Regulation by Developmental Signaling.

J Signal Transduct

Department of Pharmacology and Toxicology, Indiana University School of Medicine, IU-Melvin and Bren Simon Cancer Center, Indianapolis, IN 46202, USA.

Published: September 2015

Phosphatase and tensin homologue (PTEN) is a critical cell endogenous inhibitor of phosphoinositide signaling in mammalian cells. PTEN dephosphorylates phosphoinositide trisphosphate (PIP3), and by so doing PTEN has the function of negative regulation of Akt, thereby inhibiting this key intracellular signal transduction pathway. In numerous cell types, PTEN loss-of-function mutations result in unopposed Akt signaling, producing numerous effects on cells. Numerous reports exist regarding mutations in PTEN leading to unregulated Akt and human disease, most notably cancer. However, less is commonly known about nonmutational regulation of PTEN. This review focuses on an emerging literature on the regulation of PTEN at the transcriptional, posttranscriptional, translational, and posttranslational levels. Specifically, a focus is placed on the role developmental signaling pathways play in PTEN regulation; this includes insulin-like growth factor, NOTCH, transforming growth factor, bone morphogenetic protein, wnt, and hedgehog signaling. The regulation of PTEN by developmental mediators affects critical biological processes including neuronal and organ development, stem cell maintenance, cell cycle regulation, inflammation, response to hypoxia, repair and recovery, and cell death and survival. Perturbations of PTEN regulation consequently lead to human diseases such as cancer, chronic inflammatory syndromes, developmental abnormalities, diabetes, and neurodegeneration.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539077PMC
http://dx.doi.org/10.1155/2015/282567DOI Listing

Publication Analysis

Top Keywords

regulation pten
12
pten
10
phosphatase tensin
8
tensin homologue
8
regulation
8
developmental signaling
8
pten regulation
8
growth factor
8
signaling
5
cell
5

Similar Publications

PTEN loss in glioma cell lines leads to increased extracellular vesicle biogenesis and PD-L1 cargo in a PI3K-dependent manner.

J Biol Chem

December 2024

Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA; Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, 14853, USA. Electronic address:

Phosphatase and Tensin Homologue (PTEN) is one of the most frequently lost tumor suppressors in cancer and the predominant negative regulator of the PI3K/AKT signaling axis. A growing body of evidence has highlighted the loss of PTEN with immuno-modulatory functions including the upregulation of the programmed death ligand-1 (PD-L1), an altered tumor derived secretome that drives an immunosuppressive tumor immune microenvironment (TIME), and resistance to certain immunotherapies. Given their roles in immunosuppression and tumor growth, we examined whether the loss of PTEN would impact the biogenesis, cargo, and function of extracellular vesicles (EVs) in the context of the anti-tumor associated cytokine interferon-γ (IFN-γ).

View Article and Find Full Text PDF

Anti-miR21-conjugated DNA nanohydrogel for enhanced cancer therapy.

Biomater Adv

December 2024

Department of Chemistry and the Natural Science Research Institute, Myongji University, 116 Myongji-ro, Yongin-si 17058, Republic of Korea. Electronic address:

MicroRNAs (miRNAs) are non-coding, endogenous small single-stranded RNA molecules involved in post-transcriptional regulation of gene expression. It has been demonstrated that dysregulation of miRNA plays a major role in tumor formation, proliferation, and metastasis. Therefore, the delivery of anti-miRNA oligonucleotides to block the activity of these oncogenic miRNAs is a high-potential anti-cancer therapy approach.

View Article and Find Full Text PDF

Backgrounds: Recent studies have proven the oncogenic role of kinesin family member 20A () in several cancers. Tumor-associated macrophages (TAMs) were reported to participate in tumor initiation and metastasis. In this study, we aimed to explore the detailed mechanism underlying in regulating the progression of ovarian cancer and its involvement with TAMs.

View Article and Find Full Text PDF

Background: Chronic obstructive pulmonary disease (COPD) is a prevalent yet manageable respiratory condition. However, treatments presently used normally have side effects and cannot cure COPD, making it urgent to explore effective medications. The ginsenoside Rg3 (Rg3) has been shown to have anti-inflammatory and anti-tumor properties and can improve COPD.

View Article and Find Full Text PDF

[Parkin deletion affects PINK1/Parkin-mediated mitochondrial autophagy to exacerbate neuroinflammation and accelerate progression of Parkinson's disease in mice].

Nan Fang Yi Ke Da Xue Xue Bao

December 2024

Anhui Provincial Center for Neural Regeneration Technology and New Medical Materials Engineering Research, Bengbu Medical University, Bengbu 233000, China.

Objectives: To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD).

Methods: Wild-type (WT) male C57BL/6 mice and Parkin mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting.

View Article and Find Full Text PDF

Want 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!