Cancer progression by the okadaic acid class of tumor promoters and endogenous protein inhibitors of PP2A, SET and CIP2A
Purpose Okadaic acid class of tumor promoters are transformed into endogenous protein inhibitors of PP2A, SET, and CIP2A in human cancers. This indicates that inhibition of PP2A activity is a common mechanism of cancer progression in humans. It is important to study the roles of SET and CIP2A vis-à-...
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Veröffentlicht in: | Journal of cancer research and clinical oncology 2023-09, Vol.149 (11), p.9425-9433 |
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container_title | Journal of cancer research and clinical oncology |
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creator | Fujiki, Hirota Sueoka, Eisaburo Watanabe, Tatsuro Komori, Atsumasa Suganuma, Masami |
description | Purpose
Okadaic acid class of tumor promoters are transformed into endogenous protein inhibitors of PP2A, SET, and CIP2A in human cancers. This indicates that inhibition of PP2A activity is a common mechanism of cancer progression in humans. It is important to study the roles of SET and CIP2A vis-à-vis their clinical significance on the basis of new information gathered from a search of PubMed.
Results and discussion
The first part of this review introduces the carcinogenic roles of TNF-α and IL-1, which are induced by the okadaic acid class of compounds. The second part describes unique features of SET and CIP2A in cancer progression for several types of human cancer: (1) SET-expressing circulating tumor cells (SET-CTCs) in breast cancer, (2) knockdown of CIP2A and increased PP2A activity in chronic myeloid leukemia, (3) CIP2A and epidermal growth factor receptor (EGFR) activity in erlotinib sensitive- and resistant-non-small cell lung cancer, (4) SET antagonist EMQA plus radiation therapy against hepatocellular carcinoma, (5) PP2A inactivation as a common event in colorectal cancer, (6) prostate cancer susceptibility variants, homeobox transcription factor (
HOXB13
T) and
CIP2A
T, and (7) SET inhibitor OP449 for pre-clinical investigation of pancreatic cancer. In the Discussion, the binding complex of SET is briefly introduced, and overexpression of SET and CIP2A proteins is discussed in relation to age-associated chronic inflammation (inflammaging).
Conclusion
This review establishes the concept that inhibition of PP2A activity is a common mechanism of human cancer progression and activation of PP2A activity leads to effective anticancer therapy. |
doi_str_mv | 10.1007/s00432-023-04800-4 |
format | Article |
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Okadaic acid class of tumor promoters are transformed into endogenous protein inhibitors of PP2A, SET, and CIP2A in human cancers. This indicates that inhibition of PP2A activity is a common mechanism of cancer progression in humans. It is important to study the roles of SET and CIP2A vis-à-vis their clinical significance on the basis of new information gathered from a search of PubMed.
Results and discussion
The first part of this review introduces the carcinogenic roles of TNF-α and IL-1, which are induced by the okadaic acid class of compounds. The second part describes unique features of SET and CIP2A in cancer progression for several types of human cancer: (1) SET-expressing circulating tumor cells (SET-CTCs) in breast cancer, (2) knockdown of CIP2A and increased PP2A activity in chronic myeloid leukemia, (3) CIP2A and epidermal growth factor receptor (EGFR) activity in erlotinib sensitive- and resistant-non-small cell lung cancer, (4) SET antagonist EMQA plus radiation therapy against hepatocellular carcinoma, (5) PP2A inactivation as a common event in colorectal cancer, (6) prostate cancer susceptibility variants, homeobox transcription factor (
HOXB13
T) and
CIP2A
T, and (7) SET inhibitor OP449 for pre-clinical investigation of pancreatic cancer. In the Discussion, the binding complex of SET is briefly introduced, and overexpression of SET and CIP2A proteins is discussed in relation to age-associated chronic inflammation (inflammaging).
Conclusion
This review establishes the concept that inhibition of PP2A activity is a common mechanism of human cancer progression and activation of PP2A activity leads to effective anticancer therapy.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-023-04800-4</identifier><identifier>PMID: 37097392</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Autoantigens - metabolism ; Breast cancer ; Cancer ; Cancer Research ; Carcinogens ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Cell Line, Tumor ; Chronic myeloid leukemia ; Colorectal carcinoma ; Epidermal growth factor receptors ; Hematology ; Hepatocellular carcinoma ; Homeobox ; Humans ; Interleukin 1 ; Internal Medicine ; Intracellular Signaling Peptides and Proteins - genetics ; Liver Neoplasms ; Lung Neoplasms - drug therapy ; Male ; Medicine ; Medicine & Public Health ; Membrane Proteins - metabolism ; Myeloid leukemia ; Non-small cell lung carcinoma ; Okadaic Acid ; Oncology ; Pancreatic cancer ; Promoters ; Prostate cancer ; Radiation therapy ; Review ; Small cell lung carcinoma ; Tumor cells ; Tumor necrosis factor-α ; Tumors</subject><ispartof>Journal of cancer research and clinical oncology, 2023-09, Vol.149 (11), p.9425-9433</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-8cce63af4e385c5c5118a2729b16bb311bcc6e0d3018fe78c1206808f73964e23</citedby><cites>FETCH-LOGICAL-c541t-8cce63af4e385c5c5118a2729b16bb311bcc6e0d3018fe78c1206808f73964e23</cites><orcidid>0000-0002-1512-3551</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-023-04800-4$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-023-04800-4$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37097392$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujiki, Hirota</creatorcontrib><creatorcontrib>Sueoka, Eisaburo</creatorcontrib><creatorcontrib>Watanabe, Tatsuro</creatorcontrib><creatorcontrib>Komori, Atsumasa</creatorcontrib><creatorcontrib>Suganuma, Masami</creatorcontrib><title>Cancer progression by the okadaic acid class of tumor promoters and endogenous protein inhibitors of PP2A, SET and CIP2A</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
Okadaic acid class of tumor promoters are transformed into endogenous protein inhibitors of PP2A, SET, and CIP2A in human cancers. This indicates that inhibition of PP2A activity is a common mechanism of cancer progression in humans. It is important to study the roles of SET and CIP2A vis-à-vis their clinical significance on the basis of new information gathered from a search of PubMed.
Results and discussion
The first part of this review introduces the carcinogenic roles of TNF-α and IL-1, which are induced by the okadaic acid class of compounds. The second part describes unique features of SET and CIP2A in cancer progression for several types of human cancer: (1) SET-expressing circulating tumor cells (SET-CTCs) in breast cancer, (2) knockdown of CIP2A and increased PP2A activity in chronic myeloid leukemia, (3) CIP2A and epidermal growth factor receptor (EGFR) activity in erlotinib sensitive- and resistant-non-small cell lung cancer, (4) SET antagonist EMQA plus radiation therapy against hepatocellular carcinoma, (5) PP2A inactivation as a common event in colorectal cancer, (6) prostate cancer susceptibility variants, homeobox transcription factor (
HOXB13
T) and
CIP2A
T, and (7) SET inhibitor OP449 for pre-clinical investigation of pancreatic cancer. In the Discussion, the binding complex of SET is briefly introduced, and overexpression of SET and CIP2A proteins is discussed in relation to age-associated chronic inflammation (inflammaging).
Conclusion
This review establishes the concept that inhibition of PP2A activity is a common mechanism of human cancer progression and activation of PP2A activity leads to effective anticancer therapy.</description><subject>Autoantigens - metabolism</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Carcinogens</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Cell Line, Tumor</subject><subject>Chronic myeloid leukemia</subject><subject>Colorectal carcinoma</subject><subject>Epidermal growth factor receptors</subject><subject>Hematology</subject><subject>Hepatocellular carcinoma</subject><subject>Homeobox</subject><subject>Humans</subject><subject>Interleukin 1</subject><subject>Internal Medicine</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Liver Neoplasms</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Proteins - metabolism</subject><subject>Myeloid leukemia</subject><subject>Non-small cell lung carcinoma</subject><subject>Okadaic Acid</subject><subject>Oncology</subject><subject>Pancreatic cancer</subject><subject>Promoters</subject><subject>Prostate cancer</subject><subject>Radiation therapy</subject><subject>Review</subject><subject>Small cell lung carcinoma</subject><subject>Tumor cells</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU9v1DAQxS0EokvhC3BAlrhwIDC2E9s5oWpVoFIlKlHOluNMdl0Se7ETRL893t1S_hyQD9Z4fvPGT4-Q5wzeMAD1NgPUglfARQW1BqjqB2TF9k9MiOYhWQFTrGo4kyfkSc43UOpG8cfkRCholWj5ivxY2-Aw0V2Km4Q5-xhod0vnLdL41fbWO2qd76kbbc40DnRepnjApzhjytSGnmLo4wZDXPK-MaMP1Iet7_wc02Ho6oqfvaafz68P-PqilE_Jo8GOGZ_d3afky_vz6_XH6vLTh4v12WXlmprNlXYOpbBDjUI3rhzGtOWKtx2TXScY65yTCL0ApgdU2jEOUoMeij1ZIxen5N1Rd7d0E_YOw5zsaHbJTzbdmmi9-bsT_NZs4nfDQKhatm1ReHWnkOK3BfNsJp8djqMNWCwbrkGC4lLrgr78B72JSwrFX6FqLtsGmCwUP1IuxZwTDve_YWD2yZpjsqYkaw7JmroMvfjTx_3IrygLII5ALq2wwfR7939kfwJTNK5E</recordid><startdate>20230901</startdate><enddate>20230901</enddate><creator>Fujiki, Hirota</creator><creator>Sueoka, Eisaburo</creator><creator>Watanabe, Tatsuro</creator><creator>Komori, Atsumasa</creator><creator>Suganuma, Masami</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1512-3551</orcidid></search><sort><creationdate>20230901</creationdate><title>Cancer progression by the okadaic acid class of tumor promoters and endogenous protein inhibitors of PP2A, SET and CIP2A</title><author>Fujiki, Hirota ; Sueoka, Eisaburo ; Watanabe, Tatsuro ; Komori, Atsumasa ; Suganuma, Masami</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-8cce63af4e385c5c5118a2729b16bb311bcc6e0d3018fe78c1206808f73964e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Autoantigens - metabolism</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Carcinogens</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Cell Line, Tumor</topic><topic>Chronic myeloid leukemia</topic><topic>Colorectal carcinoma</topic><topic>Epidermal growth factor receptors</topic><topic>Hematology</topic><topic>Hepatocellular carcinoma</topic><topic>Homeobox</topic><topic>Humans</topic><topic>Interleukin 1</topic><topic>Internal Medicine</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Liver Neoplasms</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane Proteins - metabolism</topic><topic>Myeloid leukemia</topic><topic>Non-small cell lung carcinoma</topic><topic>Okadaic Acid</topic><topic>Oncology</topic><topic>Pancreatic cancer</topic><topic>Promoters</topic><topic>Prostate cancer</topic><topic>Radiation therapy</topic><topic>Review</topic><topic>Small cell lung carcinoma</topic><topic>Tumor cells</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujiki, Hirota</creatorcontrib><creatorcontrib>Sueoka, Eisaburo</creatorcontrib><creatorcontrib>Watanabe, Tatsuro</creatorcontrib><creatorcontrib>Komori, Atsumasa</creatorcontrib><creatorcontrib>Suganuma, Masami</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujiki, Hirota</au><au>Sueoka, Eisaburo</au><au>Watanabe, Tatsuro</au><au>Komori, Atsumasa</au><au>Suganuma, Masami</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer progression by the okadaic acid class of tumor promoters and endogenous protein inhibitors of PP2A, SET and CIP2A</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2023-09-01</date><risdate>2023</risdate><volume>149</volume><issue>11</issue><spage>9425</spage><epage>9433</epage><pages>9425-9433</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
Okadaic acid class of tumor promoters are transformed into endogenous protein inhibitors of PP2A, SET, and CIP2A in human cancers. This indicates that inhibition of PP2A activity is a common mechanism of cancer progression in humans. It is important to study the roles of SET and CIP2A vis-à-vis their clinical significance on the basis of new information gathered from a search of PubMed.
Results and discussion
The first part of this review introduces the carcinogenic roles of TNF-α and IL-1, which are induced by the okadaic acid class of compounds. The second part describes unique features of SET and CIP2A in cancer progression for several types of human cancer: (1) SET-expressing circulating tumor cells (SET-CTCs) in breast cancer, (2) knockdown of CIP2A and increased PP2A activity in chronic myeloid leukemia, (3) CIP2A and epidermal growth factor receptor (EGFR) activity in erlotinib sensitive- and resistant-non-small cell lung cancer, (4) SET antagonist EMQA plus radiation therapy against hepatocellular carcinoma, (5) PP2A inactivation as a common event in colorectal cancer, (6) prostate cancer susceptibility variants, homeobox transcription factor (
HOXB13
T) and
CIP2A
T, and (7) SET inhibitor OP449 for pre-clinical investigation of pancreatic cancer. In the Discussion, the binding complex of SET is briefly introduced, and overexpression of SET and CIP2A proteins is discussed in relation to age-associated chronic inflammation (inflammaging).
Conclusion
This review establishes the concept that inhibition of PP2A activity is a common mechanism of human cancer progression and activation of PP2A activity leads to effective anticancer therapy.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37097392</pmid><doi>10.1007/s00432-023-04800-4</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-1512-3551</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Autoantigens - metabolism Breast cancer Cancer Cancer Research Carcinogens Carcinoma, Non-Small-Cell Lung - drug therapy Cell Line, Tumor Chronic myeloid leukemia Colorectal carcinoma Epidermal growth factor receptors Hematology Hepatocellular carcinoma Homeobox Humans Interleukin 1 Internal Medicine Intracellular Signaling Peptides and Proteins - genetics Liver Neoplasms Lung Neoplasms - drug therapy Male Medicine Medicine & Public Health Membrane Proteins - metabolism Myeloid leukemia Non-small cell lung carcinoma Okadaic Acid Oncology Pancreatic cancer Promoters Prostate cancer Radiation therapy Review Small cell lung carcinoma Tumor cells Tumor necrosis factor-α Tumors |
title | Cancer progression by the okadaic acid class of tumor promoters and endogenous protein inhibitors of PP2A, SET and CIP2A |
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