FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription
Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel-resistant cervical cancer. Methods. Paclitaxel-resi...
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| creator | Hou, Youxiang Dong, Zhanfei Zhong, Wei Yin, Linglong Li, Xiong Kuerban, Gulina Huang, He |
| description | Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel-resistant cervical cancer. Methods. Paclitaxel-resistant Caski cells (Caski/Taxol cells) were established by intermittently exposing the Caski cells to gradually increasing concentrations of paclitaxel. The association between FOXM1, ATP-binding cassette subfamily C member 5 (ABCC5), and cervical cancer cell drug resistance was assessed by overexpressing or knocking down the expression of FOXM1 in Caski or Caski/Taxol cells. The protein and mRNA expression levels, the ratio of cellular apoptosis, and cell migration as well as intracellular drug concentrations were measured in cells following the different treatments. Results. After the successful establishment of resistant Caski/Taxol cells, cell cycle distribution analysis showed that a significantly larger percentage of Caski/Taxol cells was in the G0/G1 stage compared with the Caski cells (P |
| doi_str_mv | 10.1155/2022/3032590 |
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| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8820921</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A697663190</galeid><sourcerecordid>A697663190</sourcerecordid><originalsourceid>FETCH-LOGICAL-c542t-9a6a9184c7100d2eea89cfb6ee5def70c83af6e93486b4c3769c54978620fe8d3</originalsourceid><addsrcrecordid>eNp9kc1rFDEYh4MottTePEvAi6Br8zHJJBdhHdsqVCpSwZMhm3lnmjKbbJOZlv73Zth1_TiYS76e90lefgg9p-QtpUKcMMLYCSecCU0eoUPGabWQtKKP92vOD9BxzjekDEUl0fIpOuCiMJyzQ_Tj7PL7Z4q_pLiOI2T8IU09_grZ59EGB9gH3EC6884OuJlPUtkPQ8arh4L102BHH3q8fN80Ap9DAHyVbMgu-c3oY3iGnnR2yHC8m4_Qt7PTq-bj4uLy_FOzvFg4UbFxoa20mqrK1ZSQlgFYpV23kgCiha4mTnHbSdC8UnJVOV5LXQp1rSQjHaiWH6F3W-9mWq2hdRDGZAezSX5t04OJ1pu_b4K_Nn28M0oxohktglc7QYq3E-TRrH12pVMbIE7ZMMnqqmZCkIK-_Ae9iVMKpb2ZUowSRvVvqrcDGB-6WN51s9Qspa6l5FTPrjdbyqWYc4Ju_2VKzJywmRM2u4QL_uLPNvfwrzwL8HoLXPvQ2nv_f91Pr3uq9Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2628210219</pqid></control><display><type>article</type><title>FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription</title><source>MEDLINE</source><source>PubMed Central Open Access</source><source>Wiley Online Library Open Access</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Hou, Youxiang ; Dong, Zhanfei ; Zhong, Wei ; Yin, Linglong ; Li, Xiong ; Kuerban, Gulina ; Huang, He</creator><contributor>Upham, Brad ; Brad Upham</contributor><creatorcontrib>Hou, Youxiang ; Dong, Zhanfei ; Zhong, Wei ; Yin, Linglong ; Li, Xiong ; Kuerban, Gulina ; Huang, He ; Upham, Brad ; Brad Upham</creatorcontrib><description>Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel-resistant cervical cancer. Methods. Paclitaxel-resistant Caski cells (Caski/Taxol cells) were established by intermittently exposing the Caski cells to gradually increasing concentrations of paclitaxel. The association between FOXM1, ATP-binding cassette subfamily C member 5 (ABCC5), and cervical cancer cell drug resistance was assessed by overexpressing or knocking down the expression of FOXM1 in Caski or Caski/Taxol cells. The protein and mRNA expression levels, the ratio of cellular apoptosis, and cell migration as well as intracellular drug concentrations were measured in cells following the different treatments. Results. After the successful establishment of resistant Caski/Taxol cells, cell cycle distribution analysis showed that a significantly larger percentage of Caski/Taxol cells was in the G0/G1 stage compared with the Caski cells (P<0.01), whereas a significantly larger percentage of Caski cells was in the S and G2/M stage compared with the Caski/Taxol cells following treatment with paclitaxel (P<0.01). Both the protein and mRNA expression levels of FOXM1 and ABCC5 transporters were significantly higher in the paclitaxel-resistant Caski/Taxol cells compared with Caski cells (P<0.05). Knockdown of FOXM1 significantly lowered the protein expression levels of FOXM1 and ABCC5. Intracellular paclitaxel concentrations were significantly higher amongst the Caski/Taxol cells following the knockdown of FOXM1 by shRNA or Siomycin A (P<0.05). Conclusion. FOXM1 promotes drug resistance in cervical cancer cells by regulating ABCC5 gene transcription. The knockdown of FOXM1 with shRNA or Siomycin A promotes paclitaxel-induced cell death by regulating ABCC5 gene transcription.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2022/3032590</identifier><identifier>PMID: 35141332</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Cancer ; Cancer therapies ; Cell culture ; Cell cycle ; Cell Cycle - drug effects ; Cell death ; Cell division ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cervical cancer ; Cervix ; Cloning ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Drug therapy ; Female ; Flow cytometry ; Forkhead Box Protein M1 - genetics ; Forkhead protein ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Health aspects ; Humans ; Intracellular ; Laboratories ; Membrane proteins ; Membranes ; Multidrug Resistance-Associated Proteins - genetics ; Paclitaxel ; Paclitaxel - pharmacology ; Physiological aspects ; Proteins ; Siomycin A ; Target recognition ; Taxol ; Transcription ; Transcription, Genetic - drug effects ; Uterine Cervical Neoplasms - genetics ; Wound healing</subject><ispartof>BioMed research international, 2022, Vol.2022 (1), p.3032590-3032590</ispartof><rights>Copyright © 2022 Youxiang Hou et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 Youxiang Hou 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 Youxiang Hou et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-9a6a9184c7100d2eea89cfb6ee5def70c83af6e93486b4c3769c54978620fe8d3</citedby><cites>FETCH-LOGICAL-c542t-9a6a9184c7100d2eea89cfb6ee5def70c83af6e93486b4c3769c54978620fe8d3</cites><orcidid>0000-0002-4682-8335 ; 0000-0003-3904-3238 ; 0000-0001-5188-529X</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/PMC8820921/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8820921/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35141332$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Upham, Brad</contributor><contributor>Brad Upham</contributor><creatorcontrib>Hou, Youxiang</creatorcontrib><creatorcontrib>Dong, Zhanfei</creatorcontrib><creatorcontrib>Zhong, Wei</creatorcontrib><creatorcontrib>Yin, Linglong</creatorcontrib><creatorcontrib>Li, Xiong</creatorcontrib><creatorcontrib>Kuerban, Gulina</creatorcontrib><creatorcontrib>Huang, He</creatorcontrib><title>FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel-resistant cervical cancer. Methods. Paclitaxel-resistant Caski cells (Caski/Taxol cells) were established by intermittently exposing the Caski cells to gradually increasing concentrations of paclitaxel. The association between FOXM1, ATP-binding cassette subfamily C member 5 (ABCC5), and cervical cancer cell drug resistance was assessed by overexpressing or knocking down the expression of FOXM1 in Caski or Caski/Taxol cells. The protein and mRNA expression levels, the ratio of cellular apoptosis, and cell migration as well as intracellular drug concentrations were measured in cells following the different treatments. Results. After the successful establishment of resistant Caski/Taxol cells, cell cycle distribution analysis showed that a significantly larger percentage of Caski/Taxol cells was in the G0/G1 stage compared with the Caski cells (P<0.01), whereas a significantly larger percentage of Caski cells was in the S and G2/M stage compared with the Caski/Taxol cells following treatment with paclitaxel (P<0.01). Both the protein and mRNA expression levels of FOXM1 and ABCC5 transporters were significantly higher in the paclitaxel-resistant Caski/Taxol cells compared with Caski cells (P<0.05). Knockdown of FOXM1 significantly lowered the protein expression levels of FOXM1 and ABCC5. Intracellular paclitaxel concentrations were significantly higher amongst the Caski/Taxol cells following the knockdown of FOXM1 by shRNA or Siomycin A (P<0.05). Conclusion. FOXM1 promotes drug resistance in cervical cancer cells by regulating ABCC5 gene transcription. The knockdown of FOXM1 with shRNA or Siomycin A promotes paclitaxel-induced cell death by regulating ABCC5 gene transcription.</description><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell death</subject><subject>Cell division</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Cloning</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Forkhead Box Protein M1 - genetics</subject><subject>Forkhead protein</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Intracellular</subject><subject>Laboratories</subject><subject>Membrane proteins</subject><subject>Membranes</subject><subject>Multidrug Resistance-Associated Proteins - genetics</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Siomycin A</subject><subject>Target recognition</subject><subject>Taxol</subject><subject>Transcription</subject><subject>Transcription, Genetic - drug effects</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Wound healing</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1rFDEYh4MottTePEvAi6Br8zHJJBdhHdsqVCpSwZMhm3lnmjKbbJOZlv73Zth1_TiYS76e90lefgg9p-QtpUKcMMLYCSecCU0eoUPGabWQtKKP92vOD9BxzjekDEUl0fIpOuCiMJyzQ_Tj7PL7Z4q_pLiOI2T8IU09_grZ59EGB9gH3EC6884OuJlPUtkPQ8arh4L102BHH3q8fN80Ap9DAHyVbMgu-c3oY3iGnnR2yHC8m4_Qt7PTq-bj4uLy_FOzvFg4UbFxoa20mqrK1ZSQlgFYpV23kgCiha4mTnHbSdC8UnJVOV5LXQp1rSQjHaiWH6F3W-9mWq2hdRDGZAezSX5t04OJ1pu_b4K_Nn28M0oxohktglc7QYq3E-TRrH12pVMbIE7ZMMnqqmZCkIK-_Ae9iVMKpb2ZUowSRvVvqrcDGB-6WN51s9Qspa6l5FTPrjdbyqWYc4Ju_2VKzJywmRM2u4QL_uLPNvfwrzwL8HoLXPvQ2nv_f91Pr3uq9Q</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Hou, Youxiang</creator><creator>Dong, Zhanfei</creator><creator>Zhong, Wei</creator><creator>Yin, Linglong</creator><creator>Li, Xiong</creator><creator>Kuerban, Gulina</creator><creator>Huang, He</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4682-8335</orcidid><orcidid>https://orcid.org/0000-0003-3904-3238</orcidid><orcidid>https://orcid.org/0000-0001-5188-529X</orcidid></search><sort><creationdate>2022</creationdate><title>FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription</title><author>Hou, Youxiang ; Dong, Zhanfei ; Zhong, Wei ; Yin, Linglong ; Li, Xiong ; Kuerban, Gulina ; Huang, He</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c542t-9a6a9184c7100d2eea89cfb6ee5def70c83af6e93486b4c3769c54978620fe8d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell death</topic><topic>Cell division</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cervical cancer</topic><topic>Cervix</topic><topic>Cloning</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Forkhead Box Protein M1 - genetics</topic><topic>Forkhead protein</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Intracellular</topic><topic>Laboratories</topic><topic>Membrane proteins</topic><topic>Membranes</topic><topic>Multidrug Resistance-Associated Proteins - genetics</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Siomycin A</topic><topic>Target recognition</topic><topic>Taxol</topic><topic>Transcription</topic><topic>Transcription, Genetic - drug effects</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hou, Youxiang</creatorcontrib><creatorcontrib>Dong, Zhanfei</creatorcontrib><creatorcontrib>Zhong, Wei</creatorcontrib><creatorcontrib>Yin, Linglong</creatorcontrib><creatorcontrib>Li, Xiong</creatorcontrib><creatorcontrib>Kuerban, Gulina</creatorcontrib><creatorcontrib>Huang, He</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>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hou, Youxiang</au><au>Dong, Zhanfei</au><au>Zhong, Wei</au><au>Yin, Linglong</au><au>Li, Xiong</au><au>Kuerban, Gulina</au><au>Huang, He</au><au>Upham, Brad</au><au>Brad Upham</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><issue>1</issue><spage>3032590</spage><epage>3032590</epage><pages>3032590-3032590</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Objective. The aim of the present study was to investigate the effect of forkhead box M1 (FOXM1) to paclitaxel resistance in cervical cancer cells, to determine the underlying mechanism, and to identify novel targets for the treatment of paclitaxel-resistant cervical cancer. Methods. Paclitaxel-resistant Caski cells (Caski/Taxol cells) were established by intermittently exposing the Caski cells to gradually increasing concentrations of paclitaxel. The association between FOXM1, ATP-binding cassette subfamily C member 5 (ABCC5), and cervical cancer cell drug resistance was assessed by overexpressing or knocking down the expression of FOXM1 in Caski or Caski/Taxol cells. The protein and mRNA expression levels, the ratio of cellular apoptosis, and cell migration as well as intracellular drug concentrations were measured in cells following the different treatments. Results. After the successful establishment of resistant Caski/Taxol cells, cell cycle distribution analysis showed that a significantly larger percentage of Caski/Taxol cells was in the G0/G1 stage compared with the Caski cells (P<0.01), whereas a significantly larger percentage of Caski cells was in the S and G2/M stage compared with the Caski/Taxol cells following treatment with paclitaxel (P<0.01). Both the protein and mRNA expression levels of FOXM1 and ABCC5 transporters were significantly higher in the paclitaxel-resistant Caski/Taxol cells compared with Caski cells (P<0.05). Knockdown of FOXM1 significantly lowered the protein expression levels of FOXM1 and ABCC5. Intracellular paclitaxel concentrations were significantly higher amongst the Caski/Taxol cells following the knockdown of FOXM1 by shRNA or Siomycin A (P<0.05). Conclusion. FOXM1 promotes drug resistance in cervical cancer cells by regulating ABCC5 gene transcription. The knockdown of FOXM1 with shRNA or Siomycin A promotes paclitaxel-induced cell death by regulating ABCC5 gene transcription.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35141332</pmid><doi>10.1155/2022/3032590</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-4682-8335</orcidid><orcidid>https://orcid.org/0000-0003-3904-3238</orcidid><orcidid>https://orcid.org/0000-0001-5188-529X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Cancer Cancer therapies Cell culture Cell cycle Cell Cycle - drug effects Cell death Cell division Cell Line, Tumor Cell migration Cell Movement - drug effects Cervical cancer Cervix Cloning Drug resistance Drug Resistance, Neoplasm - genetics Drug therapy Female Flow cytometry Forkhead Box Protein M1 - genetics Forkhead protein Gene expression Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Health aspects Humans Intracellular Laboratories Membrane proteins Membranes Multidrug Resistance-Associated Proteins - genetics Paclitaxel Paclitaxel - pharmacology Physiological aspects Proteins Siomycin A Target recognition Taxol Transcription Transcription, Genetic - drug effects Uterine Cervical Neoplasms - genetics Wound healing |
| title | FOXM1 Promotes Drug Resistance in Cervical Cancer Cells by Regulating ABCC5 Gene Transcription |
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