CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming
Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secre...
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| Veröffentlicht in: | Animal cells and systems 2022, 26(4), , pp.148-157 |
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| creator | Lu, Xiangyu Wu, Yilei Cao, Rui Yu, Xiaojiong Gong, Jun |
| description | Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC. |
| doi_str_mv | 10.1080/19768354.2022.2091019 |
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However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.</description><identifier>ISSN: 1976-8354</identifier><identifier>EISSN: 2151-2485</identifier><identifier>DOI: 10.1080/19768354.2022.2091019</identifier><identifier>PMID: 36046033</identifier><language>eng</language><publisher>Daejeon: Taylor & Francis</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Antibodies ; Binding ; Cancer ; Chemotherapy ; Crosstalk ; CXCL12 ; CXCL12 protein ; CXCR4 protein ; Gemcitabine ; Gene expression ; Glycolysis ; Lactic acid ; Metastases ; Pancreatic cancer ; Pancreatic stellate cells ; Pheochromocytoma cells ; Proteins ; resistance ; Sensitivity ; Stellate cells ; TOR protein ; Translational Medicine ; Tumors ; 생물학</subject><ispartof>Animal Cells and Systems, 2022, 26(4), , pp.148-157</ispartof><rights>2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2022</rights><rights>2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 The Author(s). 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However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Binding</subject><subject>Cancer</subject><subject>Chemotherapy</subject><subject>Crosstalk</subject><subject>CXCL12</subject><subject>CXCL12 protein</subject><subject>CXCR4 protein</subject><subject>Gemcitabine</subject><subject>Gene expression</subject><subject>Glycolysis</subject><subject>Lactic acid</subject><subject>Metastases</subject><subject>Pancreatic cancer</subject><subject>Pancreatic stellate cells</subject><subject>Pheochromocytoma cells</subject><subject>Proteins</subject><subject>resistance</subject><subject>Sensitivity</subject><subject>Stellate cells</subject><subject>TOR protein</subject><subject>Translational Medicine</subject><subject>Tumors</subject><subject>생물학</subject><issn>1976-8354</issn><issn>2151-2485</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNp9kl2L1DAUhoso7rj6E4SCNyJ0zWcnuRGXwY-BAUFW8C6cJqfdzLbNmHSU-Qv-atOZUVwvvMlJz3nelzR5i-I5JVeUKPKa6mWtuBRXjDCWF00J1Q-KBaOSVkwo-bBYzEw1QxfFk5S2hNSMKP24uOA1ETXhfFH8XH1dbSgrE9qIE7qyOZQ7GPMHTN6WacK-hwlLm2sqweaKMTdS2eFg_QSNH7GMmHyasgzL0P6tt3MvzqY43ua9H7uy6w829Id5HHEXQxdhGPLgafGohT7hs3O9LL68f3ez-lhtPn1Yr643lZVLMVWycQobVKilo8iRKgDFtHWsaRlK5Vy-GAau0cQSDm1dO6vALSWTjCOx_LJ4dfIdY2vurDcB_LF2wdxFc_35Zm0oIZxpJTK8PsEuwNbsoh8gHo6KYyPEzkDMv9KjsYzJRjDnCBLRshqU48vWOYeukY5A9npz8trtmwGdxXGK0N8zvT8Z_W0-1HejBeOK62zw8mwQw7c9pskMPs0vAyOGfTJsSXROAREqoy_-QbdhH8d8rzNVC10zITMlT5SNIaWI7Z_DUGLmmJnfMTNzzMw5Zln39qTzYxviAD9C7J2Z4NCH2Mb5nZPh_7f4BdXY24Q</recordid><startdate>20220704</startdate><enddate>20220704</enddate><creator>Lu, Xiangyu</creator><creator>Wu, Yilei</creator><creator>Cao, Rui</creator><creator>Yu, Xiaojiong</creator><creator>Gong, Jun</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><general>한국통합생물학회</general><scope>0YH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7SN</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><scope>ACYCR</scope></search><sort><creationdate>20220704</creationdate><title>CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming</title><author>Lu, Xiangyu ; Wu, Yilei ; Cao, Rui ; Yu, Xiaojiong ; Gong, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-5bd8ebe8e95d1e3e18aa829cd2bf2e58dd7682adb90c03af66dc8ad752523e0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Binding</topic><topic>Cancer</topic><topic>Chemotherapy</topic><topic>Crosstalk</topic><topic>CXCL12</topic><topic>CXCL12 protein</topic><topic>CXCR4 protein</topic><topic>Gemcitabine</topic><topic>Gene expression</topic><topic>Glycolysis</topic><topic>Lactic acid</topic><topic>Metastases</topic><topic>Pancreatic cancer</topic><topic>Pancreatic stellate cells</topic><topic>Pheochromocytoma cells</topic><topic>Proteins</topic><topic>resistance</topic><topic>Sensitivity</topic><topic>Stellate cells</topic><topic>TOR protein</topic><topic>Translational Medicine</topic><topic>Tumors</topic><topic>생물학</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Xiangyu</creatorcontrib><creatorcontrib>Wu, Yilei</creatorcontrib><creatorcontrib>Cao, Rui</creatorcontrib><creatorcontrib>Yu, Xiaojiong</creatorcontrib><creatorcontrib>Gong, Jun</creatorcontrib><collection>Access via Taylor & Francis (Open Access Collection)</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Ecology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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 China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><collection>Korean Citation Index</collection><jtitle>Animal cells and systems</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Xiangyu</au><au>Wu, Yilei</au><au>Cao, Rui</au><au>Yu, Xiaojiong</au><au>Gong, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming</atitle><jtitle>Animal cells and systems</jtitle><date>2022-07-04</date><risdate>2022</risdate><volume>26</volume><issue>4</issue><spage>148</spage><epage>157</epage><pages>148-157</pages><issn>1976-8354</issn><eissn>2151-2485</eissn><abstract>Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.</abstract><cop>Daejeon</cop><pub>Taylor & Francis</pub><pmid>36046033</pmid><doi>10.1080/19768354.2022.2091019</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Antibodies Binding Cancer Chemotherapy Crosstalk CXCL12 CXCL12 protein CXCR4 protein Gemcitabine Gene expression Glycolysis Lactic acid Metastases Pancreatic cancer Pancreatic stellate cells Pheochromocytoma cells Proteins resistance Sensitivity Stellate cells TOR protein Translational Medicine Tumors 생물학 |
| title | CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming |
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