Nuclear MAST4 Suppresses FOXO3 through Interaction with AKT3 and Induces Chemoresistance in Pancreatic Ductal Carcinoma
Pancreatic ductal adenocarcinoma (PDAC) is highly malignant, with a 5-year survival rate of less than 10%. Furthermore, the acquisition of anticancer drug resistance makes PDAC treatment difficult. We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer...
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| Veröffentlicht in: | International journal of molecular sciences 2024-04, Vol.25 (7), p.4056 |
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| creator | Fujiwara-Tani, Rina Sasaki, Takamitsu Bhawal, Ujjal Kumar Mori, Shiori Ogata, Ruiko Sasaki, Rika Ikemoto, Ayaka Kishi, Shingo Fujii, Kiyomu Ohmori, Hitoshi Sho, Masayuki Kuniyasu, Hiroki |
| description | Pancreatic ductal adenocarcinoma (PDAC) is highly malignant, with a 5-year survival rate of less than 10%. Furthermore, the acquisition of anticancer drug resistance makes PDAC treatment difficult. We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer drug, using the human PDAC cell line-MIA-PaCa-2. Microtubule-associated serine/threonine kinase-4 (
) expression was increased in MIA-GEM cells compared with the parent cell line. Through inhibitor screening, dysregulated AKT signaling was identified in MIA-GEM cells with overexpression of AKT3.
knockdown effectively suppressed AKT3 overexpression, and both
and AKT3 translocation into the nucleus, phosphorylating forkhead box O3a (FOXO3) in MIA-GEM cells. Modulating FOXO3 target gene expression in these cells inhibited apoptosis while promoting stemness and proliferation. Notably, nuclear
demonstrated higher expression in GEM-resistant PDAC cases compared with that in the GEM-sensitive cases. Elevated
expression correlated with a poorer prognosis in PDAC. Consequently, nuclear
emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC. |
| doi_str_mv | 10.3390/ijms25074056 |
| format | Article |
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) expression was increased in MIA-GEM cells compared with the parent cell line. Through inhibitor screening, dysregulated AKT signaling was identified in MIA-GEM cells with overexpression of AKT3.
knockdown effectively suppressed AKT3 overexpression, and both
and AKT3 translocation into the nucleus, phosphorylating forkhead box O3a (FOXO3) in MIA-GEM cells. Modulating FOXO3 target gene expression in these cells inhibited apoptosis while promoting stemness and proliferation. Notably, nuclear
demonstrated higher expression in GEM-resistant PDAC cases compared with that in the GEM-sensitive cases. Elevated
expression correlated with a poorer prognosis in PDAC. Consequently, nuclear
emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25074056</identifier><identifier>PMID: 38612866</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Antineoplastic Agents ; Apoptosis ; Breast cancer ; Cancer ; Cancer therapies ; Carcinoma, Pancreatic Ductal - drug therapy ; Carcinoma, Pancreatic Ductal - genetics ; Care and treatment ; Cells ; Comparative analysis ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Forkhead Box Protein O3 - genetics ; Gemcitabine ; Gene expression ; Genes ; Health aspects ; Humans ; Kinases ; Medical prognosis ; Microtubule-Associated Proteins ; Microtubules ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Phosphorylation ; Protein Serine-Threonine Kinases ; Proteins ; Proto-Oncogene Proteins c-akt ; Scientific equipment and supplies industry</subject><ispartof>International journal of molecular sciences, 2024-04, Vol.25 (7), p.4056</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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><cites>FETCH-LOGICAL-c381t-70f12291190731e52e9ad16a9a1a9572a21eeb293d9e854b8397b4c19ff7fc943</cites><orcidid>0000-0002-3746-009X ; 0000-0003-2298-8825</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38612866$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujiwara-Tani, Rina</creatorcontrib><creatorcontrib>Sasaki, Takamitsu</creatorcontrib><creatorcontrib>Bhawal, Ujjal Kumar</creatorcontrib><creatorcontrib>Mori, Shiori</creatorcontrib><creatorcontrib>Ogata, Ruiko</creatorcontrib><creatorcontrib>Sasaki, Rika</creatorcontrib><creatorcontrib>Ikemoto, Ayaka</creatorcontrib><creatorcontrib>Kishi, Shingo</creatorcontrib><creatorcontrib>Fujii, Kiyomu</creatorcontrib><creatorcontrib>Ohmori, Hitoshi</creatorcontrib><creatorcontrib>Sho, Masayuki</creatorcontrib><creatorcontrib>Kuniyasu, Hiroki</creatorcontrib><title>Nuclear MAST4 Suppresses FOXO3 through Interaction with AKT3 and Induces Chemoresistance in Pancreatic Ductal Carcinoma</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Pancreatic ductal adenocarcinoma (PDAC) is highly malignant, with a 5-year survival rate of less than 10%. Furthermore, the acquisition of anticancer drug resistance makes PDAC treatment difficult. We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer drug, using the human PDAC cell line-MIA-PaCa-2. Microtubule-associated serine/threonine kinase-4 (
) expression was increased in MIA-GEM cells compared with the parent cell line. Through inhibitor screening, dysregulated AKT signaling was identified in MIA-GEM cells with overexpression of AKT3.
knockdown effectively suppressed AKT3 overexpression, and both
and AKT3 translocation into the nucleus, phosphorylating forkhead box O3a (FOXO3) in MIA-GEM cells. Modulating FOXO3 target gene expression in these cells inhibited apoptosis while promoting stemness and proliferation. Notably, nuclear
demonstrated higher expression in GEM-resistant PDAC cases compared with that in the GEM-sensitive cases. Elevated
expression correlated with a poorer prognosis in PDAC. Consequently, nuclear
emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC.</description><subject>Antineoplastic Agents</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Care and treatment</subject><subject>Cells</subject><subject>Comparative analysis</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Forkhead Box Protein O3 - genetics</subject><subject>Gemcitabine</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Microtubule-Associated Proteins</subject><subject>Microtubules</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Phosphorylation</subject><subject>Protein Serine-Threonine Kinases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Scientific equipment and supplies industry</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkctrGzEQxkVIyPvWcxH00kOd6LFarY7GbdrQJC7EhdwWWTsby-xKrh6E_veRSdomJcxhhpnfNwzzIfSOkjPOFTm36zEyQWRFRL2DDmnF2ISQWu6-qA_QUYxrQhhnQu2jA97UlDV1fYgebrIZQAd8Pb1dVPg2bzYBYoSIL-Z3c47TKvh8v8KXLkHQJlnv8INNKzz9vuBYu65MumwKP1vB6IvWxqSdAWwd_lGKADpZgz9nk_SAZzoY6_yoT9Ber4cIp8_5GP28-LKYfZtczb9ezqZXE8MbmiaS9JQxRakiklMQDJTuaK2VploJyTSjAEumeKegEdWy4UouK0NV38veqIofo49PezfB_8oQUzvaaGAYtAOfY8sJbyouJOUF_fAfuvY5uHLdlpKiYUJW_6h7PUBrXe9T-ct2aTuVihCqGG8KdfYGVaKD0RrvoLel_0rw6Ulggo8xQN9ugh11-N1S0m59bl_6XPD3z7fm5QjdX_iPsfwRIS2gaQ</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Fujiwara-Tani, Rina</creator><creator>Sasaki, Takamitsu</creator><creator>Bhawal, Ujjal Kumar</creator><creator>Mori, Shiori</creator><creator>Ogata, Ruiko</creator><creator>Sasaki, Rika</creator><creator>Ikemoto, Ayaka</creator><creator>Kishi, Shingo</creator><creator>Fujii, Kiyomu</creator><creator>Ohmori, Hitoshi</creator><creator>Sho, Masayuki</creator><creator>Kuniyasu, Hiroki</creator><general>MDPI AG</general><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>7X7</scope><scope>7XB</scope><scope>88E</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3746-009X</orcidid><orcidid>https://orcid.org/0000-0003-2298-8825</orcidid></search><sort><creationdate>20240401</creationdate><title>Nuclear MAST4 Suppresses FOXO3 through Interaction with AKT3 and Induces Chemoresistance in Pancreatic Ductal Carcinoma</title><author>Fujiwara-Tani, Rina ; Sasaki, Takamitsu ; Bhawal, Ujjal Kumar ; Mori, Shiori ; Ogata, Ruiko ; Sasaki, Rika ; Ikemoto, Ayaka ; Kishi, Shingo ; Fujii, Kiyomu ; Ohmori, Hitoshi ; Sho, Masayuki ; Kuniyasu, Hiroki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-70f12291190731e52e9ad16a9a1a9572a21eeb293d9e854b8397b4c19ff7fc943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antineoplastic Agents</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Pancreatic Ductal - drug therapy</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Care and treatment</topic><topic>Cells</topic><topic>Comparative analysis</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Forkhead Box Protein O3 - genetics</topic><topic>Gemcitabine</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Medical prognosis</topic><topic>Microtubule-Associated Proteins</topic><topic>Microtubules</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Phosphorylation</topic><topic>Protein Serine-Threonine Kinases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Scientific equipment and supplies industry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujiwara-Tani, Rina</creatorcontrib><creatorcontrib>Sasaki, Takamitsu</creatorcontrib><creatorcontrib>Bhawal, Ujjal Kumar</creatorcontrib><creatorcontrib>Mori, Shiori</creatorcontrib><creatorcontrib>Ogata, Ruiko</creatorcontrib><creatorcontrib>Sasaki, Rika</creatorcontrib><creatorcontrib>Ikemoto, Ayaka</creatorcontrib><creatorcontrib>Kishi, Shingo</creatorcontrib><creatorcontrib>Fujii, Kiyomu</creatorcontrib><creatorcontrib>Ohmori, Hitoshi</creatorcontrib><creatorcontrib>Sho, Masayuki</creatorcontrib><creatorcontrib>Kuniyasu, Hiroki</creatorcontrib><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>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</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</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujiwara-Tani, Rina</au><au>Sasaki, Takamitsu</au><au>Bhawal, Ujjal Kumar</au><au>Mori, Shiori</au><au>Ogata, Ruiko</au><au>Sasaki, Rika</au><au>Ikemoto, Ayaka</au><au>Kishi, Shingo</au><au>Fujii, Kiyomu</au><au>Ohmori, Hitoshi</au><au>Sho, Masayuki</au><au>Kuniyasu, Hiroki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nuclear MAST4 Suppresses FOXO3 through Interaction with AKT3 and Induces Chemoresistance in Pancreatic Ductal Carcinoma</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-04-01</date><risdate>2024</risdate><volume>25</volume><issue>7</issue><spage>4056</spage><pages>4056-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Pancreatic ductal adenocarcinoma (PDAC) is highly malignant, with a 5-year survival rate of less than 10%. Furthermore, the acquisition of anticancer drug resistance makes PDAC treatment difficult. We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer drug, using the human PDAC cell line-MIA-PaCa-2. Microtubule-associated serine/threonine kinase-4 (
) expression was increased in MIA-GEM cells compared with the parent cell line. Through inhibitor screening, dysregulated AKT signaling was identified in MIA-GEM cells with overexpression of AKT3.
knockdown effectively suppressed AKT3 overexpression, and both
and AKT3 translocation into the nucleus, phosphorylating forkhead box O3a (FOXO3) in MIA-GEM cells. Modulating FOXO3 target gene expression in these cells inhibited apoptosis while promoting stemness and proliferation. Notably, nuclear
demonstrated higher expression in GEM-resistant PDAC cases compared with that in the GEM-sensitive cases. Elevated
expression correlated with a poorer prognosis in PDAC. Consequently, nuclear
emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38612866</pmid><doi>10.3390/ijms25074056</doi><orcidid>https://orcid.org/0000-0002-3746-009X</orcidid><orcidid>https://orcid.org/0000-0003-2298-8825</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents Apoptosis Breast cancer Cancer Cancer therapies Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Care and treatment Cells Comparative analysis Drug resistance Drug Resistance, Neoplasm - genetics Forkhead Box Protein O3 - genetics Gemcitabine Gene expression Genes Health aspects Humans Kinases Medical prognosis Microtubule-Associated Proteins Microtubules Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Phosphorylation Protein Serine-Threonine Kinases Proteins Proto-Oncogene Proteins c-akt Scientific equipment and supplies industry |
| title | Nuclear MAST4 Suppresses FOXO3 through Interaction with AKT3 and Induces Chemoresistance in Pancreatic Ductal Carcinoma |
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