Phosphatase and tensin homologue deleted on chromosome 10.

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor gene deleted or mutated in many human cancers such as glioblastoma, spinal tumors, prostate, bladder, adrenals, thyroid, breast, endometrium, and colon cancers. They result from loss of heterozygosity (LOH) for the PTEN gene on chromosome 10q23. Previous studies reported that various drugs, chemicals, and foods can up-regulate PTEN mRNA and protein expression in different cell lines, and they may be useful in the future prevention and/or treatment of these cancers. PTEN has also been observed to have prognostic significance and is gradually being accepted as an independent prognostic factor. This will help in monitoring disease progression and/or recurrence, with a view to improving treatment outcomes and reducing the associated morbidity and mortality from these cancers. Neprilysin (NEP) is a zinc-dependent metallopeptidase that cleaves and inactivates some biologically active peptides thus switching off signal transduction at the cell surface. Decreased NEP expression in many cancers has been reported. NEP can form a complex with PTEN and enhance PTEN recruitment to the plasma membrane as well as stabilize its phosphatase activity. MicroRNA-21 (miR-21) post-transcriptionally down-regulates the expression of PTEN and stimulates growth and invasion in non-small cell lung cancer (NSCLC) (lung Ca), suggesting that this may be a potential therapeutic target in the future treatment of NSCLC. PTEN is a tumor suppressor gene associated with many human cancers. This has diagnostic, therapeutic, and prognostic significance in the management of many human cancers, and may be a target for new drug development in the future.