Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway
Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) fie...
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creator | Tsai, Cheng-Yu Ko, Huey-Jiun Huang, Chi-Ying F. Lin, Ching-Yi Chiou, Shean-Jaw Su, Yu-Feng Lieu, Ann-Shung Loh, Joon-Khim Kwan, Aij-Lie Chuang, Tsung-Hsien Hong, Yi-Ren |
description | Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. This study offers a new therapeutic strategy for targeting GBM in the future. |
doi_str_mv | 10.3390/life11050451 |
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Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. This study offers a new therapeutic strategy for targeting GBM in the future.</description><identifier>ISSN: 2075-1729</identifier><identifier>EISSN: 2075-1729</identifier><identifier>DOI: 10.3390/life11050451</identifier><identifier>PMID: 34069945</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Antibodies ; Autophagy ; Cancer ; Cancer therapies ; CD44 antigen ; Chemoradiotherapy ; Chemotherapy ; CSC ; GBM ; Gene expression ; Glioblastoma ; Glioblastoma multiforme ; GSC ; Hypoxia ; Ionizing radiation ; ionizing radiation (IR) ; Markers ; Medical prognosis ; Medical research ; Nestin ; Phagocytosis ; Phenotypes ; Proteasome inhibitors ; Proteins ; Radiation ; Radiation standards ; Radiation tolerance ; Radioresistance ; Stem cells ; Tumorigenesis ; Wnt protein ; Wnt/β-Catenin ; β-Catenin</subject><ispartof>Life (Basel, Switzerland), 2021-05, Vol.11 (5), p.451</ispartof><rights>2021 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><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-4f7880f01408d44ca96d3eb9c94c7adf1c009819276b6316ad7710ebb909a16d3</citedby><cites>FETCH-LOGICAL-c455t-4f7880f01408d44ca96d3eb9c94c7adf1c009819276b6316ad7710ebb909a16d3</cites><orcidid>0000-0002-0539-8201</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/PMC8157563/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8157563/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>Tsai, Cheng-Yu</creatorcontrib><creatorcontrib>Ko, Huey-Jiun</creatorcontrib><creatorcontrib>Huang, Chi-Ying F.</creatorcontrib><creatorcontrib>Lin, Ching-Yi</creatorcontrib><creatorcontrib>Chiou, Shean-Jaw</creatorcontrib><creatorcontrib>Su, Yu-Feng</creatorcontrib><creatorcontrib>Lieu, Ann-Shung</creatorcontrib><creatorcontrib>Loh, Joon-Khim</creatorcontrib><creatorcontrib>Kwan, Aij-Lie</creatorcontrib><creatorcontrib>Chuang, Tsung-Hsien</creatorcontrib><creatorcontrib>Hong, Yi-Ren</creatorcontrib><title>Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway</title><title>Life (Basel, Switzerland)</title><description>Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. This study offers a new therapeutic strategy for targeting GBM in the future.</description><subject>Antibodies</subject><subject>Autophagy</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>CD44 antigen</subject><subject>Chemoradiotherapy</subject><subject>Chemotherapy</subject><subject>CSC</subject><subject>GBM</subject><subject>Gene expression</subject><subject>Glioblastoma</subject><subject>Glioblastoma multiforme</subject><subject>GSC</subject><subject>Hypoxia</subject><subject>Ionizing radiation</subject><subject>ionizing radiation (IR)</subject><subject>Markers</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Nestin</subject><subject>Phagocytosis</subject><subject>Phenotypes</subject><subject>Proteasome inhibitors</subject><subject>Proteins</subject><subject>Radiation</subject><subject>Radiation standards</subject><subject>Radiation tolerance</subject><subject>Radioresistance</subject><subject>Stem cells</subject><subject>Tumorigenesis</subject><subject>Wnt protein</subject><subject>Wnt/β-Catenin</subject><subject>β-Catenin</subject><issn>2075-1729</issn><issn>2075-1729</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><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>eNpdkl9rFDEQwBdRbKl98wMEfPHBtckmm2xehHJoPTiwVMXHMPmzdzl3kzPJtpwfyw_iZ3LPK9I6LzPM_PgxDFNVLwl-S6nEF4PvHSG4xawlT6rTBou2JqKRTx_UJ9V5zls8B28J79jz6oQyzKVk7Wl1t4zB__RhjW7Aeig-BrQMdjIuoxuXfS4QCroafNQD5BJHQJ-LG-uV_-7Qwg1DRnqPrlMcYzlYLqcSdxtY79GtB1Q2Dn0L5eL3r3oBxQUf0DWUzR3sX1TPehiyO7_PZ9XXD--_LD7Wq09Xy8XlqjasbUvNetF1uMeE4c4yZkByS52WRjIjwPbEYCw7IhvBNaeEgxWCYKe1xBLIzJ5Vy6PXRtiqXfIjpL2K4NXfRkxrBal4MzjFNQhrKeeGScZ7DT221GosuOWk72F2vTu6dpMenTUulATDI-njSfAbtY63qiOtaDmdBa_vBSn-mFwuavTZzEeE4OKUVdNSzjpOJJnRV_-h2zilMJ_qQDWMNA0XM_XmSJkUc06u_7cMwerwIOrhg9A_DpGupA</recordid><startdate>20210518</startdate><enddate>20210518</enddate><creator>Tsai, Cheng-Yu</creator><creator>Ko, Huey-Jiun</creator><creator>Huang, Chi-Ying F.</creator><creator>Lin, Ching-Yi</creator><creator>Chiou, Shean-Jaw</creator><creator>Su, Yu-Feng</creator><creator>Lieu, Ann-Shung</creator><creator>Loh, Joon-Khim</creator><creator>Kwan, Aij-Lie</creator><creator>Chuang, Tsung-Hsien</creator><creator>Hong, Yi-Ren</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</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>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0539-8201</orcidid></search><sort><creationdate>20210518</creationdate><title>Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway</title><author>Tsai, Cheng-Yu ; Ko, Huey-Jiun ; Huang, Chi-Ying F. ; Lin, Ching-Yi ; Chiou, Shean-Jaw ; Su, Yu-Feng ; Lieu, Ann-Shung ; Loh, Joon-Khim ; Kwan, Aij-Lie ; Chuang, Tsung-Hsien ; Hong, Yi-Ren</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-4f7880f01408d44ca96d3eb9c94c7adf1c009819276b6316ad7710ebb909a16d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antibodies</topic><topic>Autophagy</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>CD44 antigen</topic><topic>Chemoradiotherapy</topic><topic>Chemotherapy</topic><topic>CSC</topic><topic>GBM</topic><topic>Gene expression</topic><topic>Glioblastoma</topic><topic>Glioblastoma multiforme</topic><topic>GSC</topic><topic>Hypoxia</topic><topic>Ionizing radiation</topic><topic>ionizing radiation (IR)</topic><topic>Markers</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Nestin</topic><topic>Phagocytosis</topic><topic>Phenotypes</topic><topic>Proteasome inhibitors</topic><topic>Proteins</topic><topic>Radiation</topic><topic>Radiation standards</topic><topic>Radiation tolerance</topic><topic>Radioresistance</topic><topic>Stem cells</topic><topic>Tumorigenesis</topic><topic>Wnt protein</topic><topic>Wnt/β-Catenin</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsai, Cheng-Yu</creatorcontrib><creatorcontrib>Ko, Huey-Jiun</creatorcontrib><creatorcontrib>Huang, Chi-Ying F.</creatorcontrib><creatorcontrib>Lin, Ching-Yi</creatorcontrib><creatorcontrib>Chiou, Shean-Jaw</creatorcontrib><creatorcontrib>Su, Yu-Feng</creatorcontrib><creatorcontrib>Lieu, Ann-Shung</creatorcontrib><creatorcontrib>Loh, Joon-Khim</creatorcontrib><creatorcontrib>Kwan, Aij-Lie</creatorcontrib><creatorcontrib>Chuang, Tsung-Hsien</creatorcontrib><creatorcontrib>Hong, Yi-Ren</creatorcontrib><collection>CrossRef</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>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>Environmental Science Database</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>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Life (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsai, Cheng-Yu</au><au>Ko, Huey-Jiun</au><au>Huang, Chi-Ying F.</au><au>Lin, Ching-Yi</au><au>Chiou, Shean-Jaw</au><au>Su, Yu-Feng</au><au>Lieu, Ann-Shung</au><au>Loh, Joon-Khim</au><au>Kwan, Aij-Lie</au><au>Chuang, Tsung-Hsien</au><au>Hong, Yi-Ren</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway</atitle><jtitle>Life (Basel, Switzerland)</jtitle><date>2021-05-18</date><risdate>2021</risdate><volume>11</volume><issue>5</issue><spage>451</spage><pages>451-</pages><issn>2075-1729</issn><eissn>2075-1729</eissn><abstract>Therapeutic resistance in recurrent glioblastoma multiforme (GBM) after concurrent chemoradiotherapy (CCRT) is a challenging issue. Although standard fractionated radiation is essential to treat GBM, it has led to local recurrence along with therapy-resistant cells in the ionizing radiation (IR) field. Lines of evidence showed cancer stem cells (CSCs) play a vital role in therapy resistance in many cancer types, including GBM. However, the molecular mechanism is poorly understood. Here, we proposed that autophagy could be involved in GSC induction for radioresistance. In a clinical setting, patients who received radiation/chemotherapy had higher LC3II expression and showed poor overall survival compared with those with low LC3 II. In a cell model, U87MG and GBM8401 expressed high level of stemness markers CD133, CD44, Nestin, and autophagy marker P62/LC3II after receiving standard fractionated IR. Furthermore, Wnt/β-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132). Moreover, pharmacological inhibition of autophagy with BAF and CQ inhibit GSC cell growth by impairing autophagy flux as demonstrated by decrease Nestin, CD133, and SOX-2 levels. In conclusion, we demonstrated that fractionated IR could induce GSCs with the stemness phenotype by P62-mediated autophagy through the Wnt/β-catenin for radioresistance. This study offers a new therapeutic strategy for targeting GBM in the future.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>34069945</pmid><doi>10.3390/life11050451</doi><orcidid>https://orcid.org/0000-0002-0539-8201</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies Autophagy Cancer Cancer therapies CD44 antigen Chemoradiotherapy Chemotherapy CSC GBM Gene expression Glioblastoma Glioblastoma multiforme GSC Hypoxia Ionizing radiation ionizing radiation (IR) Markers Medical prognosis Medical research Nestin Phagocytosis Phenotypes Proteasome inhibitors Proteins Radiation Radiation standards Radiation tolerance Radioresistance Stem cells Tumorigenesis Wnt protein Wnt/β-Catenin β-Catenin |
title | Ionizing Radiation Induces Resistant Glioblastoma Stem-Like Cells by Promoting Autophagy via the Wnt/β-Catenin Pathway |
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