AKT as a Therapeutic Target for Cancer
Many cellular processes in cancer are attributed to kinase signaling networks. V-akt murine thymoma viral oncogene homolog (AKT) plays a major role in the PI3K/AKT signaling pathways. AKT is activated by PI3K or phosphoinositide-dependent kinases (PDK) as well as growth factors, inflammation, and DN...
Gespeichert in:
Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2019-03, Vol.79 (6), p.1019-1031 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1031 |
---|---|
container_issue | 6 |
container_start_page | 1019 |
container_title | Cancer research (Chicago, Ill.) |
container_volume | 79 |
creator | Song, Mengqiu Bode, Ann M Dong, Zigang Lee, Mee-Hyun |
description | Many cellular processes in cancer are attributed to kinase signaling networks. V-akt murine thymoma viral oncogene homolog (AKT) plays a major role in the PI3K/AKT signaling pathways. AKT is activated by PI3K or phosphoinositide-dependent kinases (PDK) as well as growth factors, inflammation, and DNA damage. Signal transduction occurs through downstream effectors such as mTOR, glycogen synthase kinase 3 beta (GSK3β), or forkhead box protein O1 (FOXO1). The abnormal overexpression or activation of AKT has been observed in many cancers, including ovarian, lung, and pancreatic cancers, and is associated with increased cancer cell proliferation and survival. Therefore, targeting AKT could provide an important approach for cancer prevention and therapy. In this review, we discuss the rationale for targeting AKT and also provide details regarding synthetic and natural AKT-targeting compounds and their associated studies. |
doi_str_mv | 10.1158/0008-5472.CAN-18-2738 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2186620276</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2186620276</sourcerecordid><originalsourceid>FETCH-LOGICAL-c526t-b0cd1ab3ae4d067e487b656a9862589ae74fc3f22cf12d3bf15b5bdc476ebd303</originalsourceid><addsrcrecordid>eNo9kMtOwzAQRS0EoqXwCaCsEBsXv-0uq4iXqGAT1pbtjKEobYqdLPh7ErV0NRrp3Bndg9A1JXNKpbknhBgshWbzcvmGqcFMc3OCplRyg7UQ8hRNj8wEXeT8PaySEnmOJpwYYpRmU3S7fK0KlwtXVF-Q3A76bh2KyqVP6IrYpqJ02wDpEp1F12S4OswZ-nh8qMpnvHp_eimXKxwkUx32JNTUee5A1ERpEEZ7JZVbGMWkWTjQIgYeGQuRspr7SKWXvg5CK_A1J3yG7vZ3d6n96SF3drPOAZrGbaHts2XUKMUI02pA5R4Nqc05QbS7tN649GspsaMiO9a3Y307KLLU2FHRkLs5vOj9Bupj6t8J_wPj6F_h</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2186620276</pqid></control><display><type>article</type><title>AKT as a Therapeutic Target for Cancer</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Song, Mengqiu ; Bode, Ann M ; Dong, Zigang ; Lee, Mee-Hyun</creator><creatorcontrib>Song, Mengqiu ; Bode, Ann M ; Dong, Zigang ; Lee, Mee-Hyun</creatorcontrib><description>Many cellular processes in cancer are attributed to kinase signaling networks. V-akt murine thymoma viral oncogene homolog (AKT) plays a major role in the PI3K/AKT signaling pathways. AKT is activated by PI3K or phosphoinositide-dependent kinases (PDK) as well as growth factors, inflammation, and DNA damage. Signal transduction occurs through downstream effectors such as mTOR, glycogen synthase kinase 3 beta (GSK3β), or forkhead box protein O1 (FOXO1). The abnormal overexpression or activation of AKT has been observed in many cancers, including ovarian, lung, and pancreatic cancers, and is associated with increased cancer cell proliferation and survival. Therefore, targeting AKT could provide an important approach for cancer prevention and therapy. In this review, we discuss the rationale for targeting AKT and also provide details regarding synthetic and natural AKT-targeting compounds and their associated studies.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-18-2738</identifier><identifier>PMID: 30808672</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antineoplastic Agents - therapeutic use ; Humans ; Molecular Targeted Therapy ; Neoplasms - drug therapy ; Neoplasms - metabolism ; Neoplasms - pathology ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><ispartof>Cancer research (Chicago, Ill.), 2019-03, Vol.79 (6), p.1019-1031</ispartof><rights>2019 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-b0cd1ab3ae4d067e487b656a9862589ae74fc3f22cf12d3bf15b5bdc476ebd303</citedby><cites>FETCH-LOGICAL-c526t-b0cd1ab3ae4d067e487b656a9862589ae74fc3f22cf12d3bf15b5bdc476ebd303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30808672$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Mengqiu</creatorcontrib><creatorcontrib>Bode, Ann M</creatorcontrib><creatorcontrib>Dong, Zigang</creatorcontrib><creatorcontrib>Lee, Mee-Hyun</creatorcontrib><title>AKT as a Therapeutic Target for Cancer</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Many cellular processes in cancer are attributed to kinase signaling networks. V-akt murine thymoma viral oncogene homolog (AKT) plays a major role in the PI3K/AKT signaling pathways. AKT is activated by PI3K or phosphoinositide-dependent kinases (PDK) as well as growth factors, inflammation, and DNA damage. Signal transduction occurs through downstream effectors such as mTOR, glycogen synthase kinase 3 beta (GSK3β), or forkhead box protein O1 (FOXO1). The abnormal overexpression or activation of AKT has been observed in many cancers, including ovarian, lung, and pancreatic cancers, and is associated with increased cancer cell proliferation and survival. Therefore, targeting AKT could provide an important approach for cancer prevention and therapy. In this review, we discuss the rationale for targeting AKT and also provide details regarding synthetic and natural AKT-targeting compounds and their associated studies.</description><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Humans</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMtOwzAQRS0EoqXwCaCsEBsXv-0uq4iXqGAT1pbtjKEobYqdLPh7ErV0NRrp3Bndg9A1JXNKpbknhBgshWbzcvmGqcFMc3OCplRyg7UQ8hRNj8wEXeT8PaySEnmOJpwYYpRmU3S7fK0KlwtXVF-Q3A76bh2KyqVP6IrYpqJ02wDpEp1F12S4OswZ-nh8qMpnvHp_eimXKxwkUx32JNTUee5A1ERpEEZ7JZVbGMWkWTjQIgYeGQuRspr7SKWXvg5CK_A1J3yG7vZ3d6n96SF3drPOAZrGbaHts2XUKMUI02pA5R4Nqc05QbS7tN649GspsaMiO9a3Y307KLLU2FHRkLs5vOj9Bupj6t8J_wPj6F_h</recordid><startdate>20190315</startdate><enddate>20190315</enddate><creator>Song, Mengqiu</creator><creator>Bode, Ann M</creator><creator>Dong, Zigang</creator><creator>Lee, Mee-Hyun</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20190315</creationdate><title>AKT as a Therapeutic Target for Cancer</title><author>Song, Mengqiu ; Bode, Ann M ; Dong, Zigang ; Lee, Mee-Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-b0cd1ab3ae4d067e487b656a9862589ae74fc3f22cf12d3bf15b5bdc476ebd303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Humans</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-akt - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Mengqiu</creatorcontrib><creatorcontrib>Bode, Ann M</creatorcontrib><creatorcontrib>Dong, Zigang</creatorcontrib><creatorcontrib>Lee, Mee-Hyun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Mengqiu</au><au>Bode, Ann M</au><au>Dong, Zigang</au><au>Lee, Mee-Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AKT as a Therapeutic Target for Cancer</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2019-03-15</date><risdate>2019</risdate><volume>79</volume><issue>6</issue><spage>1019</spage><epage>1031</epage><pages>1019-1031</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><abstract>Many cellular processes in cancer are attributed to kinase signaling networks. V-akt murine thymoma viral oncogene homolog (AKT) plays a major role in the PI3K/AKT signaling pathways. AKT is activated by PI3K or phosphoinositide-dependent kinases (PDK) as well as growth factors, inflammation, and DNA damage. Signal transduction occurs through downstream effectors such as mTOR, glycogen synthase kinase 3 beta (GSK3β), or forkhead box protein O1 (FOXO1). The abnormal overexpression or activation of AKT has been observed in many cancers, including ovarian, lung, and pancreatic cancers, and is associated with increased cancer cell proliferation and survival. Therefore, targeting AKT could provide an important approach for cancer prevention and therapy. In this review, we discuss the rationale for targeting AKT and also provide details regarding synthetic and natural AKT-targeting compounds and their associated studies.</abstract><cop>United States</cop><pmid>30808672</pmid><doi>10.1158/0008-5472.CAN-18-2738</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0008-5472 |
ispartof | Cancer research (Chicago, Ill.), 2019-03, Vol.79 (6), p.1019-1031 |
issn | 0008-5472 1538-7445 |
language | eng |
recordid | cdi_proquest_miscellaneous_2186620276 |
source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Animals Antineoplastic Agents - therapeutic use Humans Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Proto-Oncogene Proteins c-akt - antagonists & inhibitors |
title | AKT as a Therapeutic Target for Cancer |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T06%3A05%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=AKT%20as%20a%20Therapeutic%20Target%20for%20Cancer&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=Song,%20Mengqiu&rft.date=2019-03-15&rft.volume=79&rft.issue=6&rft.spage=1019&rft.epage=1031&rft.pages=1019-1031&rft.issn=0008-5472&rft.eissn=1538-7445&rft_id=info:doi/10.1158/0008-5472.CAN-18-2738&rft_dat=%3Cproquest_cross%3E2186620276%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2186620276&rft_id=info:pmid/30808672&rfr_iscdi=true |