The functions of tumor suppressor PTEN in innate and adaptive immunity

Abstract

The tumor suppressor phosphatase and tensin homolog (PTEN) is a lipid and protein phosphatase that is able to antagonize the PI3K/AKT pathway and inhibit tumor growth. PTEN also possesses phosphatase-independent functions. Genetic alterations of PTEN may lead to the deregulation of cell proliferation, survival, differentiation, energy metabolism and cellular architecture and mobility. Although the role of PTEN in tumor suppression is extensively documented and well established, the evidence for its roles in immunity did not start to accumulate until recently. In this review, we will focus on the newly discovered functions of PTEN in the regulation of innate and adaptive immunity, including antiviral responses.

miR‐298 plays a pivotal role in colon cancer invasiveness by targeting PTEN

“…The Cox regression analysis was carried out for the calculation of the miR-298 prognostic score in CRC ( (Nitulescu et al, 2018;Pópulo, Lopes, & Soares, 2012). Moreover, as a lipid phosphatase, PTEN is shown to have a distinctive role in both innate and adaptive immunity (Chen & Guo, 2017;Li et al, 2016).…”

A network analysis to identify mediators of germline-driven differences in breast cancer prognosis

“…From the module-level analysis, another enriched main process was the pathway linked to PTEN (phosphatase and tensin homolog deleted on chromosome 10) regulation, which is a wellcharacterized tumor suppressor 59 . PTEN is directly involved in the metabolism of phospholipids and lipoproteins 60 , adaptive immune system, and B cell receptor associated events, 61 which were all hits in the downstream analysis. One of the six genes in the module, HEXIM1 (hexamethylene bisacetamide-inducible protein 1), is a positive regulator of p53 and has been identified as a potential novel therapeutic target modulating cell death in breast cancer cells 62 .…”

Analysis of Copy Number Loss of the ErbB4 Receptor Tyrosine Kinase in Glioblastoma

“…Loss of a tumor suppressor gene, such as PTEN, and amplification of a protooncogene, such as EGFR, both lead to cancer progression but through different mechanisms 1,2,4,12 . When a tumor suppressor is lost, it is no longer able to quell cell proliferation or induce cell death 12 ; and when a proto-oncogene is gained, amplified cell proliferation or inability to induce death occurs 1,2 . While a large volume of publicly available copy number data is generated using microarray and next-generation sequencing technologies 13,14,15 , much work remains in processing this data and interpreting the functional impacts of specific CNV's in human disease 10 .…”

“…CNV's can play an important role in human disease-by altering the structure or abundance of transcripts and proteins, for example-or can have no phenotypic effect 10,11 . Examples in many human cancers include copy number loss of the gene that codes for the tumor suppressor protein PTEN 4,12 and copy number gain in the gene that codes for the proto-oncogene EGFR 2 . Loss of a tumor suppressor gene, such as PTEN, and amplification of a protooncogene, such as EGFR, both lead to cancer progression but through different mechanisms 1,2,4,12 .…”

“…Examples in many human cancers include copy number loss of the gene that codes for the tumor suppressor protein PTEN 4,12 and copy number gain in the gene that codes for the proto-oncogene EGFR 2 . Loss of a tumor suppressor gene, such as PTEN, and amplification of a protooncogene, such as EGFR, both lead to cancer progression but through different mechanisms 1,2,4,12 . When a tumor suppressor is lost, it is no longer able to quell cell proliferation or induce cell death 12 ; and when a proto-oncogene is gained, amplified cell proliferation or inability to induce death occurs 1,2 .…”