FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway
Objective. The aim of the study is to investigate the role and possible mechanism of fascin-1 (FSCN1) in the invasion, migration, glycolysis, and epithelial-mesenchymal transition (EMT) of prostate cancer. Methods. Real-time quantitative polymerase chain reaction (qRT-PCR) was utilized to determine...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2022-06, Vol.2022, p.1-9 |
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| creator | Li, Minghui Gao, Zhiming Ding, Honglin Wang, Zhanhua Mu, Hada Zhang, Lei Wei, Jiufu Ma, Zhanshu |
| description | Objective. The aim of the study is to investigate the role and possible mechanism of fascin-1 (FSCN1) in the invasion, migration, glycolysis, and epithelial-mesenchymal transition (EMT) of prostate cancer. Methods. Real-time quantitative polymerase chain reaction (qRT-PCR) was utilized to determine the mRNA expression level of FSCN1 in prostate cancer tissues and prostate cancer cells PC-3 and DU145. The transwell and the scratch test were applied to detect the invasion and migration abilities of cells, respectively. A metabolic assay was used for measuring the glucose consumption, lactate production, and the extracellular acidification rate (ECAR) in cells; western blot was used for checking FSCN1, EMT, and yes-associated protein/transcriptional co-activators with the PDZ-binding motif (YAP/TAZ) signaling pathway-related protein expression level in cells or tissues. Results. FSCN1 was significantly highly expressed in prostate cancer tissues and cells. On the one hand, interference with the expression of FSCN1 could inhibit the invasion, migration, EMT, and glycolysis of prostate cancer cells. On the other hand, overexpression of FSCN1 promoted the invasion, migration, EMT, and glycolysis of prostate cancer cells. Besides, further mechanistic studies revealed that FSCN1 could activate the YAP/TAZ signaling pathway in prostate cancer cells. Conclusion. FSCN1 promotes invasion, migration, EMT, and glycolysis in prostate cancer cells by activating the YAP/TAZ signaling pathway. FSCN1 may be used as a biomarker for the diagnosis or treatment in prostate cancer. |
| doi_str_mv | 10.1155/2022/6245647 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9259215</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2688091200</sourcerecordid><originalsourceid>FETCH-LOGICAL-c425t-d99729836b42005e581135a8a734e4383214e7a3afc966302e392ca8fea8fdf3</originalsourceid><addsrcrecordid>eNp9kV9rFDEUxQdRbK2--QECvgg6bv5MJpkXYVnaWqi60H1QX8LtTGYnJZOsSaZlvr3Z7lLQBx8uuZBfDifnFMVbgj8RwvmCYkoXNa14XYlnxSkRFSkrKuXzp138OClexXiHMW2EEC-LE8Yl4bSWp8X9xc3qG0Hr4EefdESXdm69naOJCFyHzncmDdoasOVXHbVrh3kEizYBXDTJeIeM2z-OCZJGK3CtDigNwU_bAQH6uVwvNstf6MZsHVjjtmgNaXiA-XXxogcb9ZvjeVZsLs43qy_l9ffLq9XyumwrylPZNY2gjWT1bUUx5jrbJoyDBMEqXTHJKKm0AAZ929Q1w1SzhrYge52n69lZ8fkgu5tuR9212qUAVu2CGSHMyoNRf984M6itv1cN5Q0lPAu8PwoE_3vSManRxFZbC077KaqcocQNyeYy-u4f9M5PIX_7kRKcUVyTTH08UG0OLQbdP5khWO37VPs-1bHPjH844INxHTyY_9N_AMbmnhc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2687532061</pqid></control><display><type>article</type><title>FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Li, Minghui ; Gao, Zhiming ; Ding, Honglin ; Wang, Zhanhua ; Mu, Hada ; Zhang, Lei ; Wei, Jiufu ; Ma, Zhanshu</creator><contributor>Zia-Ul-Haq, Muhammad ; Muhammad Zia-Ul-Haq</contributor><creatorcontrib>Li, Minghui ; Gao, Zhiming ; Ding, Honglin ; Wang, Zhanhua ; Mu, Hada ; Zhang, Lei ; Wei, Jiufu ; Ma, Zhanshu ; Zia-Ul-Haq, Muhammad ; Muhammad Zia-Ul-Haq</creatorcontrib><description>Objective. The aim of the study is to investigate the role and possible mechanism of fascin-1 (FSCN1) in the invasion, migration, glycolysis, and epithelial-mesenchymal transition (EMT) of prostate cancer. Methods. Real-time quantitative polymerase chain reaction (qRT-PCR) was utilized to determine the mRNA expression level of FSCN1 in prostate cancer tissues and prostate cancer cells PC-3 and DU145. The transwell and the scratch test were applied to detect the invasion and migration abilities of cells, respectively. A metabolic assay was used for measuring the glucose consumption, lactate production, and the extracellular acidification rate (ECAR) in cells; western blot was used for checking FSCN1, EMT, and yes-associated protein/transcriptional co-activators with the PDZ-binding motif (YAP/TAZ) signaling pathway-related protein expression level in cells or tissues. Results. FSCN1 was significantly highly expressed in prostate cancer tissues and cells. On the one hand, interference with the expression of FSCN1 could inhibit the invasion, migration, EMT, and glycolysis of prostate cancer cells. On the other hand, overexpression of FSCN1 promoted the invasion, migration, EMT, and glycolysis of prostate cancer cells. Besides, further mechanistic studies revealed that FSCN1 could activate the YAP/TAZ signaling pathway in prostate cancer cells. Conclusion. FSCN1 promotes invasion, migration, EMT, and glycolysis in prostate cancer cells by activating the YAP/TAZ signaling pathway. FSCN1 may be used as a biomarker for the diagnosis or treatment in prostate cancer.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2022/6245647</identifier><identifier>PMID: 35815268</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Acidification ; Cancer therapies ; Cell adhesion & migration ; Cell migration ; Gene expression ; Glucose ; Glycolysis ; Lactic acid ; Medical prognosis ; Mesenchyme ; Metastasis ; Polymerase chain reaction ; Prostate cancer ; Proteins ; Signal transduction ; Surgery ; Transcription factors ; Yes-associated protein</subject><ispartof>Evidence-based complementary and alternative medicine, 2022-06, Vol.2022, p.1-9</ispartof><rights>Copyright © 2022 Minghui Li et al.</rights><rights>Copyright © 2022 Minghui Li 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 Minghui Li et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-d99729836b42005e581135a8a734e4383214e7a3afc966302e392ca8fea8fdf3</citedby><cites>FETCH-LOGICAL-c425t-d99729836b42005e581135a8a734e4383214e7a3afc966302e392ca8fea8fdf3</cites><orcidid>0000-0002-8368-2742</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/PMC9259215/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9259215/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids></links><search><contributor>Zia-Ul-Haq, Muhammad</contributor><contributor>Muhammad Zia-Ul-Haq</contributor><creatorcontrib>Li, Minghui</creatorcontrib><creatorcontrib>Gao, Zhiming</creatorcontrib><creatorcontrib>Ding, Honglin</creatorcontrib><creatorcontrib>Wang, Zhanhua</creatorcontrib><creatorcontrib>Mu, Hada</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Wei, Jiufu</creatorcontrib><creatorcontrib>Ma, Zhanshu</creatorcontrib><title>FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway</title><title>Evidence-based complementary and alternative medicine</title><description>Objective. The aim of the study is to investigate the role and possible mechanism of fascin-1 (FSCN1) in the invasion, migration, glycolysis, and epithelial-mesenchymal transition (EMT) of prostate cancer. Methods. Real-time quantitative polymerase chain reaction (qRT-PCR) was utilized to determine the mRNA expression level of FSCN1 in prostate cancer tissues and prostate cancer cells PC-3 and DU145. The transwell and the scratch test were applied to detect the invasion and migration abilities of cells, respectively. A metabolic assay was used for measuring the glucose consumption, lactate production, and the extracellular acidification rate (ECAR) in cells; western blot was used for checking FSCN1, EMT, and yes-associated protein/transcriptional co-activators with the PDZ-binding motif (YAP/TAZ) signaling pathway-related protein expression level in cells or tissues. Results. FSCN1 was significantly highly expressed in prostate cancer tissues and cells. On the one hand, interference with the expression of FSCN1 could inhibit the invasion, migration, EMT, and glycolysis of prostate cancer cells. On the other hand, overexpression of FSCN1 promoted the invasion, migration, EMT, and glycolysis of prostate cancer cells. Besides, further mechanistic studies revealed that FSCN1 could activate the YAP/TAZ signaling pathway in prostate cancer cells. Conclusion. FSCN1 promotes invasion, migration, EMT, and glycolysis in prostate cancer cells by activating the YAP/TAZ signaling pathway. FSCN1 may be used as a biomarker for the diagnosis or treatment in prostate cancer.</description><subject>Acidification</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glycolysis</subject><subject>Lactic acid</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Polymerase chain reaction</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Surgery</subject><subject>Transcription factors</subject><subject>Yes-associated protein</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</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>eNp9kV9rFDEUxQdRbK2--QECvgg6bv5MJpkXYVnaWqi60H1QX8LtTGYnJZOsSaZlvr3Z7lLQBx8uuZBfDifnFMVbgj8RwvmCYkoXNa14XYlnxSkRFSkrKuXzp138OClexXiHMW2EEC-LE8Yl4bSWp8X9xc3qG0Hr4EefdESXdm69naOJCFyHzncmDdoasOVXHbVrh3kEizYBXDTJeIeM2z-OCZJGK3CtDigNwU_bAQH6uVwvNstf6MZsHVjjtmgNaXiA-XXxogcb9ZvjeVZsLs43qy_l9ffLq9XyumwrylPZNY2gjWT1bUUx5jrbJoyDBMEqXTHJKKm0AAZ929Q1w1SzhrYge52n69lZ8fkgu5tuR9212qUAVu2CGSHMyoNRf984M6itv1cN5Q0lPAu8PwoE_3vSManRxFZbC077KaqcocQNyeYy-u4f9M5PIX_7kRKcUVyTTH08UG0OLQbdP5khWO37VPs-1bHPjH844INxHTyY_9N_AMbmnhc</recordid><startdate>20220629</startdate><enddate>20220629</enddate><creator>Li, Minghui</creator><creator>Gao, Zhiming</creator><creator>Ding, Honglin</creator><creator>Wang, Zhanhua</creator><creator>Mu, Hada</creator><creator>Zhang, Lei</creator><creator>Wei, Jiufu</creator><creator>Ma, Zhanshu</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</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>KB0</scope><scope>M0S</scope><scope>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8368-2742</orcidid></search><sort><creationdate>20220629</creationdate><title>FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway</title><author>Li, Minghui ; Gao, Zhiming ; Ding, Honglin ; Wang, Zhanhua ; Mu, Hada ; Zhang, Lei ; Wei, Jiufu ; Ma, Zhanshu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-d99729836b42005e581135a8a734e4383214e7a3afc966302e392ca8fea8fdf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acidification</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Glycolysis</topic><topic>Lactic acid</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Metastasis</topic><topic>Polymerase chain reaction</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Surgery</topic><topic>Transcription factors</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Minghui</creatorcontrib><creatorcontrib>Gao, Zhiming</creatorcontrib><creatorcontrib>Ding, Honglin</creatorcontrib><creatorcontrib>Wang, Zhanhua</creatorcontrib><creatorcontrib>Mu, Hada</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Wei, Jiufu</creatorcontrib><creatorcontrib>Ma, Zhanshu</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Psychology Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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 China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Evidence-based complementary and alternative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Minghui</au><au>Gao, Zhiming</au><au>Ding, Honglin</au><au>Wang, Zhanhua</au><au>Mu, Hada</au><au>Zhang, Lei</au><au>Wei, Jiufu</au><au>Ma, Zhanshu</au><au>Zia-Ul-Haq, Muhammad</au><au>Muhammad Zia-Ul-Haq</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><date>2022-06-29</date><risdate>2022</risdate><volume>2022</volume><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>Objective. The aim of the study is to investigate the role and possible mechanism of fascin-1 (FSCN1) in the invasion, migration, glycolysis, and epithelial-mesenchymal transition (EMT) of prostate cancer. Methods. Real-time quantitative polymerase chain reaction (qRT-PCR) was utilized to determine the mRNA expression level of FSCN1 in prostate cancer tissues and prostate cancer cells PC-3 and DU145. The transwell and the scratch test were applied to detect the invasion and migration abilities of cells, respectively. A metabolic assay was used for measuring the glucose consumption, lactate production, and the extracellular acidification rate (ECAR) in cells; western blot was used for checking FSCN1, EMT, and yes-associated protein/transcriptional co-activators with the PDZ-binding motif (YAP/TAZ) signaling pathway-related protein expression level in cells or tissues. Results. FSCN1 was significantly highly expressed in prostate cancer tissues and cells. On the one hand, interference with the expression of FSCN1 could inhibit the invasion, migration, EMT, and glycolysis of prostate cancer cells. On the other hand, overexpression of FSCN1 promoted the invasion, migration, EMT, and glycolysis of prostate cancer cells. Besides, further mechanistic studies revealed that FSCN1 could activate the YAP/TAZ signaling pathway in prostate cancer cells. Conclusion. FSCN1 promotes invasion, migration, EMT, and glycolysis in prostate cancer cells by activating the YAP/TAZ signaling pathway. FSCN1 may be used as a biomarker for the diagnosis or treatment in prostate cancer.</abstract><cop>New York</cop><pub>Hindawi</pub><pmid>35815268</pmid><doi>10.1155/2022/6245647</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8368-2742</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acidification Cancer therapies Cell adhesion & migration Cell migration Gene expression Glucose Glycolysis Lactic acid Medical prognosis Mesenchyme Metastasis Polymerase chain reaction Prostate cancer Proteins Signal transduction Surgery Transcription factors Yes-associated protein |
| title | FSCN1 Promotes Glycolysis and Epithelial-Mesenchymal Transition in Prostate Cancer through a YAP/TAZ Signaling Pathway |
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