PTEN is a potent tumor-suppressor protein. Aggressive and metastatic prostate cancer (PC) is associated with a reduction or loss of PTEN expression. PTEN reduction often occurs without gene mutations, and its downregulation is not fully understood. Herein, we show that PTEN is incorporated in the cargo of exosomes derived from cancer cells. PTEN is not detected in exosomes derived from normal, ...

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor that causes cell cycle arrest. Lack of a nuclear locator sequence and a function in the cytosolic phosphatidylinositol 3'-kinase/Akt pathway diverted its study from the nucleus. However, immunohistochemistry revealed PTEN in the nucleus of normal cells and decreased nuclear PTEN in neoplastic tissues. Using p...

Pten controls a signaling axis that is implicated to regulate cell proliferation, growth, survival, migration, and metabolism. The molecular mechanisms underlying the specificity of Pten responses to such diverse cellular functions are currently poorly understood. Here we report the control of Pten activity and signaling specificity during the cell cycle by Ndfip1 regulation of Pten spatial dis...

BACKGROUND Phosphatase homologue of tensin (PTEN) is the most commonly mutated gene in prostate cancer. Bone morphogenetic proteins (BMPs) are known to promote differentiation and inhibit proliferation. Previously published reports from other organ systems led us to investigate a mechanistic relationship between PTEN and BMP signaling in prostate epithelial cells. METHODS We analyzed growth r...

Pten (Phosphatase and tensin homolog deleted on chromosome 10) is a recently identified tumor suppressor gene which is deleted or mutated in a variety of primary human cancers and in three cancer predisposition syndromes [1]. Pten regulates apoptosis and cell cycle progression through its phosphatase activity on phosphatidylinositol (PI) 3,4,5-trisphosphate (PI(3,4,5)P(3)), a product of PI 3-ki...

Overexpression of c-Myc is associated with worse outcomes in endometrial cancer, indicating that c-Myc may be a promising target for endometrial cancer therapy. A novel small molecule, JQ1, has been shown to block BRD4 resulting in inhibition of c-Myc expression and tumor growth. Thus, we investigated whether JQ1 can inhibit endometrial cancer growth in cell culture and xenograft models. In PTE...

The tumor suppressor PTEN plays a critical role in the regulation of multiple cellular processes that include survival, cell cycle, proliferation and apoptosis. PTEN is frequently mutated or deleted in various human cancer cells to promote tumorigenesis. PTEN is regulated by SUMOylation, but the SUMO E3 ligase involved in the SUMOylation of PTEN remains unclear. Here, we demonstrated that PIASx...

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates the phosphoinositide-3-kinase (PI3K) signaling pathway. In colorectal cancer (CRC), observed frequencies of loss of PTEN expression, concordant expression in primary tumors and metastases, and the association of PTEN status with outcome vary markedly by detection method. We determined the degree to which PTEN ...

The tumor suppressor PTEN, a critical regulator for multiple cellular processes, is mutated or deleted frequently in various human cancers. Subtle reductions in PTEN expression levels have profound impacts on carcinogenesis. Here we show that PTEN level is regulated by ubiquitin-mediated proteasomal degradation, and purified its ubiquitin ligase as HECT-domain protein NEDD4-1. In cells NEDD4-1 ...

Objective: Stanozolol is an anabolic androgenic steroid (AAS) that widely used by teenagers and athletes in bodybuilding, sports, athletics. The potential effects of stanozolol kidney functions have not been defined. In this study we investigated the expression tumor suppressor protein phosphatase tensin homolog (Pten) mRNA levels phosphatidylinositol 4,5-bisphosphate 3 kinase (Pi3k) B (Akt1) s...