Research Progress of PI3K/PTEN/AKT Signaling Pathway Associated with Renal Cell Carcinoma
Renal cell carcinoma is a common renal malignancy of the urinary system and the most malignant type of kidney cancer. Phosphatidylinositol 3-kinase (PI3K) is an intracellular phosphatidylinositol kinase associated with oncogene products such as v-src and with serine/threonine kinase activity, and it...
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| description | Renal cell carcinoma is a common renal malignancy of the urinary system and the most malignant type of kidney cancer. Phosphatidylinositol 3-kinase (PI3K) is an intracellular phosphatidylinositol kinase associated with oncogene products such as v-src and with serine/threonine kinase activity, and its increased activity correlates with the development of several cancers. Protein kinase B (AKT) is a cyclic guanosine phosphate-dependent protein kinase that plays an important role in cell survival and apoptosis. Phosphatase and tensin homolog (PTEN), a newly discovered oncogene in recent years, participates in tumorigenesis and development by competing with tyrosine kinases for common substrates. The product encoded by PTEN was found to negatively regulate the PI3K/Akt signaling pathway, thereby inhibiting cell proliferation and promoting apoptosis. The PI3K/PTEN/AKT signaling pathway has also been identified in several studies as being involved in the development of several malignancies, including renal cell carcinoma. Radiotherapy is currently one of the most effective means of treatment for renal cell carcinoma, whereas it is predisposed to significant tolerance during the course of radiotherapy, thereby leading to treatment failure. Therefore, new treatment options may potentiate the efficiency of renal cell carcinoma treatment. With the development of tumor molecular biology, targeted biological therapy for malignant tumors has gradually become a research hotspot. Given the above research background, this study reviews the application of the PI3K/PTEN/AKT signaling pathway in renal cell carcinoma, aiming to provide more references for the treatment of clinical renal cell carcinoma. |
| doi_str_mv | 10.1155/2022/1195875 |
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Phosphatidylinositol 3-kinase (PI3K) is an intracellular phosphatidylinositol kinase associated with oncogene products such as v-src and with serine/threonine kinase activity, and its increased activity correlates with the development of several cancers. Protein kinase B (AKT) is a cyclic guanosine phosphate-dependent protein kinase that plays an important role in cell survival and apoptosis. Phosphatase and tensin homolog (PTEN), a newly discovered oncogene in recent years, participates in tumorigenesis and development by competing with tyrosine kinases for common substrates. The product encoded by PTEN was found to negatively regulate the PI3K/Akt signaling pathway, thereby inhibiting cell proliferation and promoting apoptosis. The PI3K/PTEN/AKT signaling pathway has also been identified in several studies as being involved in the development of several malignancies, including renal cell carcinoma. Radiotherapy is currently one of the most effective means of treatment for renal cell carcinoma, whereas it is predisposed to significant tolerance during the course of radiotherapy, thereby leading to treatment failure. Therefore, new treatment options may potentiate the efficiency of renal cell carcinoma treatment. With the development of tumor molecular biology, targeted biological therapy for malignant tumors has gradually become a research hotspot. Given the above research background, this study reviews the application of the PI3K/PTEN/AKT signaling pathway in renal cell carcinoma, aiming to provide more references for the treatment of clinical renal cell carcinoma.</description><identifier>ISSN: 0278-0240</identifier><identifier>ISSN: 1875-8630</identifier><identifier>EISSN: 1875-8630</identifier><identifier>DOI: 10.1155/2022/1195875</identifier><identifier>PMID: 36046376</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Apoptosis ; Cancer ; Cancer therapies ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Cell division ; Cell growth ; Cell Proliferation ; Cell survival ; Chemotherapy ; Cytotoxicity ; Drug resistance ; Esophageal cancer ; Growth factors ; Homology ; Humans ; Kidney cancer ; Kidney Neoplasms - metabolism ; Kinases ; Malignancy ; Medical prognosis ; Metastasis ; Molecular biology ; Mortality ; Pathogenesis ; Phosphatase ; Phosphatidylinositol 3-Kinase - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol kinase ; Protein-serine/threonine kinase ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Radiation therapy ; Renal cell carcinoma ; Review ; Signal Transduction ; Signaling ; Substrates ; Surgery ; Tensin ; Tumorigenesis ; Tumors ; Tyrosine</subject><ispartof>Disease markers, 2022, Vol.2022, p.1195875-4</ispartof><rights>Copyright © 2022 Yakun Fang et al.</rights><rights>Copyright © 2022 Yakun Fang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Yakun Fang et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-55cdc1467642743a79211a9a4da9a432939c8a21052caccb4602aab3a5a832283</citedby><cites>FETCH-LOGICAL-c448t-55cdc1467642743a79211a9a4da9a432939c8a21052caccb4602aab3a5a832283</cites><orcidid>0000-0003-1860-9837</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9420629/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9420629/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,4010,27904,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36046376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Shi, Zhongjie</contributor><contributor>Zhongjie Shi</contributor><creatorcontrib>Fang, Yakun</creatorcontrib><creatorcontrib>Ji, Wenjun</creatorcontrib><creatorcontrib>Yan, Chao</creatorcontrib><title>Research Progress of PI3K/PTEN/AKT Signaling Pathway Associated with Renal Cell Carcinoma</title><title>Disease markers</title><addtitle>Dis Markers</addtitle><description>Renal cell carcinoma is a common renal malignancy of the urinary system and the most malignant type of kidney cancer. Phosphatidylinositol 3-kinase (PI3K) is an intracellular phosphatidylinositol kinase associated with oncogene products such as v-src and with serine/threonine kinase activity, and its increased activity correlates with the development of several cancers. Protein kinase B (AKT) is a cyclic guanosine phosphate-dependent protein kinase that plays an important role in cell survival and apoptosis. Phosphatase and tensin homolog (PTEN), a newly discovered oncogene in recent years, participates in tumorigenesis and development by competing with tyrosine kinases for common substrates. The product encoded by PTEN was found to negatively regulate the PI3K/Akt signaling pathway, thereby inhibiting cell proliferation and promoting apoptosis. The PI3K/PTEN/AKT signaling pathway has also been identified in several studies as being involved in the development of several malignancies, including renal cell carcinoma. Radiotherapy is currently one of the most effective means of treatment for renal cell carcinoma, whereas it is predisposed to significant tolerance during the course of radiotherapy, thereby leading to treatment failure. Therefore, new treatment options may potentiate the efficiency of renal cell carcinoma treatment. With the development of tumor molecular biology, targeted biological therapy for malignant tumors has gradually become a research hotspot. Given the above research background, this study reviews the application of the PI3K/PTEN/AKT signaling pathway in renal cell carcinoma, aiming to provide more references for the treatment of clinical renal cell carcinoma.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cell survival</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Drug resistance</subject><subject>Esophageal cancer</subject><subject>Growth factors</subject><subject>Homology</subject><subject>Humans</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kinases</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Molecular biology</subject><subject>Mortality</subject><subject>Pathogenesis</subject><subject>Phosphatase</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphatidylinositol kinase</subject><subject>Protein-serine/threonine kinase</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Radiation therapy</subject><subject>Renal cell carcinoma</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Substrates</subject><subject>Surgery</subject><subject>Tensin</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Tyrosine</subject><issn>0278-0240</issn><issn>1875-8630</issn><issn>1875-8630</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNp9kcGLEzEUh4Mobq3ePEvAi6Bjk5dkJrkIpay67KJlrQdP4TWTdrK0kzWZWva_N7V1UQ9e3ju8j4_340fIc87ecq7UBBjAhHOjdKMekBEvq9K1YA_JiEGjKwaSnZEnOd8wxsFI85iciZrJWjT1iHy79tljch2dp7hOPmcaV3R-IS4n88X5p8n0ckG_hHWPm9Cv6RyHbo93dJpzdAEH39J9GDp67QtAZ35TRpGFPm7xKXm0wk32z057TL6-P1_MPlZXnz9czKZXlZNSD5VSrnVc1k0toZECGwOco0HZHoYAI4zTCJwpcOjcUtYMEJcCFWoBoMWYvDt6b3fLrW-d74eEG3ubwhbTnY0Y7N-XPnR2HX9YI4HVxT8mr06CFL_vfB7sNmRXsmDv4y5baJhhXHMDBX35D3oTd6lk_0U1UmmmD9SbI-VSzDn51f0znNlDZ_bQmT11VvAXfwa4h3-XVIDXR6ALfYv78H_dTwrbnFo</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Fang, Yakun</creator><creator>Ji, Wenjun</creator><creator>Yan, Chao</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7QL</scope><scope>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1860-9837</orcidid></search><sort><creationdate>2022</creationdate><title>Research Progress of PI3K/PTEN/AKT Signaling Pathway Associated with Renal Cell Carcinoma</title><author>Fang, Yakun ; Ji, Wenjun ; Yan, Chao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-55cdc1467642743a79211a9a4da9a432939c8a21052caccb4602aab3a5a832283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cell survival</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Drug resistance</topic><topic>Esophageal cancer</topic><topic>Growth factors</topic><topic>Homology</topic><topic>Humans</topic><topic>Kidney cancer</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kinases</topic><topic>Malignancy</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Molecular biology</topic><topic>Mortality</topic><topic>Pathogenesis</topic><topic>Phosphatase</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphatidylinositol kinase</topic><topic>Protein-serine/threonine kinase</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Radiation therapy</topic><topic>Renal cell carcinoma</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Substrates</topic><topic>Surgery</topic><topic>Tensin</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fang, Yakun</creatorcontrib><creatorcontrib>Ji, Wenjun</creatorcontrib><creatorcontrib>Yan, Chao</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Disease markers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fang, Yakun</au><au>Ji, Wenjun</au><au>Yan, Chao</au><au>Shi, Zhongjie</au><au>Zhongjie Shi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Research Progress of PI3K/PTEN/AKT Signaling Pathway Associated with Renal Cell Carcinoma</atitle><jtitle>Disease markers</jtitle><addtitle>Dis Markers</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><spage>1195875</spage><epage>4</epage><pages>1195875-4</pages><issn>0278-0240</issn><issn>1875-8630</issn><eissn>1875-8630</eissn><abstract>Renal cell carcinoma is a common renal malignancy of the urinary system and the most malignant type of kidney cancer. Phosphatidylinositol 3-kinase (PI3K) is an intracellular phosphatidylinositol kinase associated with oncogene products such as v-src and with serine/threonine kinase activity, and its increased activity correlates with the development of several cancers. Protein kinase B (AKT) is a cyclic guanosine phosphate-dependent protein kinase that plays an important role in cell survival and apoptosis. Phosphatase and tensin homolog (PTEN), a newly discovered oncogene in recent years, participates in tumorigenesis and development by competing with tyrosine kinases for common substrates. The product encoded by PTEN was found to negatively regulate the PI3K/Akt signaling pathway, thereby inhibiting cell proliferation and promoting apoptosis. The PI3K/PTEN/AKT signaling pathway has also been identified in several studies as being involved in the development of several malignancies, including renal cell carcinoma. Radiotherapy is currently one of the most effective means of treatment for renal cell carcinoma, whereas it is predisposed to significant tolerance during the course of radiotherapy, thereby leading to treatment failure. Therefore, new treatment options may potentiate the efficiency of renal cell carcinoma treatment. With the development of tumor molecular biology, targeted biological therapy for malignant tumors has gradually become a research hotspot. Given the above research background, this study reviews the application of the PI3K/PTEN/AKT signaling pathway in renal cell carcinoma, aiming to provide more references for the treatment of clinical renal cell carcinoma.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>36046376</pmid><doi>10.1155/2022/1195875</doi><tpages>4</tpages><orcidid>https://orcid.org/0000-0003-1860-9837</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Apoptosis Cancer Cancer therapies Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Cell division Cell growth Cell Proliferation Cell survival Chemotherapy Cytotoxicity Drug resistance Esophageal cancer Growth factors Homology Humans Kidney cancer Kidney Neoplasms - metabolism Kinases Malignancy Medical prognosis Metastasis Molecular biology Mortality Pathogenesis Phosphatase Phosphatidylinositol 3-Kinase - metabolism Phosphatidylinositol 3-Kinases - metabolism Phosphatidylinositol kinase Protein-serine/threonine kinase Proteins Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Radiation therapy Renal cell carcinoma Review Signal Transduction Signaling Substrates Surgery Tensin Tumorigenesis Tumors Tyrosine |
| title | Research Progress of PI3K/PTEN/AKT Signaling Pathway Associated with Renal Cell Carcinoma |
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