The mitochondrial fission factor FIS1 promotes stemness of human lung cancer stem cells via mitophagy
Mitophagy, a form of autophagy, plays a role in cancer development, progression and recurrence. Cancer stem cells (CSCs) also play a key role in these processes, although it not known whether mitophagy can regulate the stemness of CSCs. Here, we employed the A549‐SD human non‐small cell lung adenoca...
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| creator | Liu, Doudou Sun, Zhiwei Ye, Ting Li, Jingyuan Zeng, Bin Zhao, Qiting Wang, Jianyu Xing, Hongmei Rosie |
| description | Mitophagy, a form of autophagy, plays a role in cancer development, progression and recurrence. Cancer stem cells (CSCs) also play a key role in these processes, although it not known whether mitophagy can regulate the stemness of CSCs. Here, we employed the A549‐SD human non‐small cell lung adenocarcinoma CSC model that we have developed and characterized to investigate the effect of mitophagy on the stemness of CSCs. We observed a positive relationship between mitophagic activity and the stemness of lung CSCs. At the mechanistic level, our results suggest that augmentation of mitophagy in lung CSCs can be induced by FIS1 through mitochondrial fission. In addition, we assessed the clinical relevance of FIS1 in lung adenocarcinoma using The Cancer Genome Atlas database. An elevation in FIS1, when observed together with other prognostic markers for lung cancer progression, was found to correlate with shorter overall survival.
In the human non‐small cell lung adenocarcinoma cancer stem cell model A549‐SD, inhibiting the expression of FIS1 can inhibit mitochondrial division, thereby inhibiting mitophagy and consequently inhibiting the stemness of cancer stem cells. |
| doi_str_mv | 10.1002/2211-5463.13207 |
| format | Article |
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In the human non‐small cell lung adenocarcinoma cancer stem cell model A549‐SD, inhibiting the expression of FIS1 can inhibit mitochondrial division, thereby inhibiting mitophagy and consequently inhibiting the stemness of cancer stem cells.</description><identifier>ISSN: 2211-5463</identifier><identifier>EISSN: 2211-5463</identifier><identifier>DOI: 10.1002/2211-5463.13207</identifier><identifier>PMID: 34051059</identifier><language>eng</language><publisher>HOBOKEN: Wiley</publisher><subject>Adenocarcinoma ; Analysis ; Autophagy ; Biochemistry & Molecular Biology ; Cancer ; cancer stem cell ; Development and progression ; Fis1 ; Genes ; Genomes ; Humans ; Kinases ; Leukemia ; Life Sciences & Biomedicine ; Lung ; Lung cancer ; Membrane Proteins ; Metastasis ; Mitochondria ; Mitochondrial Dynamics - genetics ; mitochondrial fission ; Mitochondrial Proteins - genetics ; Mitophagy ; Neoplasms ; Neoplastic Stem Cells - pathology ; Phagocytosis ; Science & Technology ; Stem cell research ; Stem cells ; stemness ; Tumorigenesis ; Tumors ; Variance analysis</subject><ispartof>FEBS open bio, 2021-07, Vol.11 (7), p.1997-2007</ispartof><rights>2021 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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>true</woscitedreferencessubscribed><woscitedreferencescount>17</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000663297100001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c6017-e3b7c8f27b259135d3a98bff88b134ca8df653268b0658ef1a61ddba9076f6e83</citedby><cites>FETCH-LOGICAL-c6017-e3b7c8f27b259135d3a98bff88b134ca8df653268b0658ef1a61ddba9076f6e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8406485/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8406485/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,2103,2115,11567,27929,27930,39263,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34051059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Doudou</creatorcontrib><creatorcontrib>Sun, Zhiwei</creatorcontrib><creatorcontrib>Ye, Ting</creatorcontrib><creatorcontrib>Li, Jingyuan</creatorcontrib><creatorcontrib>Zeng, Bin</creatorcontrib><creatorcontrib>Zhao, Qiting</creatorcontrib><creatorcontrib>Wang, Jianyu</creatorcontrib><creatorcontrib>Xing, Hongmei Rosie</creatorcontrib><title>The mitochondrial fission factor FIS1 promotes stemness of human lung cancer stem cells via mitophagy</title><title>FEBS open bio</title><addtitle>FEBS OPEN BIO</addtitle><addtitle>FEBS Open Bio</addtitle><description>Mitophagy, a form of autophagy, plays a role in cancer development, progression and recurrence. Cancer stem cells (CSCs) also play a key role in these processes, although it not known whether mitophagy can regulate the stemness of CSCs. Here, we employed the A549‐SD human non‐small cell lung adenocarcinoma CSC model that we have developed and characterized to investigate the effect of mitophagy on the stemness of CSCs. We observed a positive relationship between mitophagic activity and the stemness of lung CSCs. At the mechanistic level, our results suggest that augmentation of mitophagy in lung CSCs can be induced by FIS1 through mitochondrial fission. In addition, we assessed the clinical relevance of FIS1 in lung adenocarcinoma using The Cancer Genome Atlas database. An elevation in FIS1, when observed together with other prognostic markers for lung cancer progression, was found to correlate with shorter overall survival.
In the human non‐small cell lung adenocarcinoma cancer stem cell model A549‐SD, inhibiting the expression of FIS1 can inhibit mitochondrial division, thereby inhibiting mitophagy and consequently inhibiting the stemness of cancer stem cells.</description><subject>Adenocarcinoma</subject><subject>Analysis</subject><subject>Autophagy</subject><subject>Biochemistry & Molecular Biology</subject><subject>Cancer</subject><subject>cancer stem cell</subject><subject>Development and progression</subject><subject>Fis1</subject><subject>Genes</subject><subject>Genomes</subject><subject>Humans</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Life Sciences & Biomedicine</subject><subject>Lung</subject><subject>Lung cancer</subject><subject>Membrane Proteins</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Mitochondrial Dynamics - genetics</subject><subject>mitochondrial fission</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitophagy</subject><subject>Neoplasms</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Phagocytosis</subject><subject>Science & Technology</subject><subject>Stem cell research</subject><subject>Stem cells</subject><subject>stemness</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Variance analysis</subject><issn>2211-5463</issn><issn>2211-5463</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>HGBXW</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><sourceid>DOA</sourceid><recordid>eNqNks9v0zAUxyMEYtPYmRuyxAUJtfPvOBekUa1QaRIHxtlyHDt1ldjFTob63-M0pdq4gH2w9fx5X79nf4viLYJLBCG-wRihBaOcLBHBsHxRXJ4jL5_sL4rrlHYwDw4Rh_B1cUEoZAiy6rIwD1sDejcEvQ2-iU51wLqUXPDAKj2ECNab7wjsY-jDYBJIg-m9SQkEC7ZjrzzoRt8Crbw28XgKtOm6BB6dOurut6o9vCleWdUlc31ar4of67uH1dfF_bcvm9Xt_ULn0sqFIXWphcVljVmFCGuIqkRtrRA1IlQr0VjOCOaihpwJY5HiqGlqVcGSW24EuSo2s24T1E7uo-tVPMignDwGQmylioPTnZFEmFoITBC2DSWWV4xnOUwbWlcM6SZrfZq19mPdm0YbP0TVPRN9fuLdVrbhUQoKORUsC3w4CcTwczRpkL1L0-Mob8KYJGaEclhVYqr7_V_oLozR56fKFBUElZRVmVrOVKtyA87bkO_VeTamdzp4Y12O35Yofy0v6SR7MyfoGFKKxp6rR1BOFpKTSeRkEnm0UM5497TpM__HMBkQM_DL1MEm7Uz--DM2eYwTXJVoshtauUEN2UqrMPohp378_9RM8xOdmzr8q3C5vvtM5xZ-AwL-8Fc</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Liu, Doudou</creator><creator>Sun, Zhiwei</creator><creator>Ye, Ting</creator><creator>Li, Jingyuan</creator><creator>Zeng, Bin</creator><creator>Zhao, Qiting</creator><creator>Wang, Jianyu</creator><creator>Xing, Hongmei Rosie</creator><general>Wiley</general><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</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>IAO</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>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>202107</creationdate><title>The mitochondrial fission factor FIS1 promotes stemness of human lung cancer stem cells via mitophagy</title><author>Liu, Doudou ; Sun, Zhiwei ; Ye, Ting ; Li, Jingyuan ; Zeng, Bin ; Zhao, Qiting ; Wang, Jianyu ; Xing, Hongmei Rosie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6017-e3b7c8f27b259135d3a98bff88b134ca8df653268b0658ef1a61ddba9076f6e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenocarcinoma</topic><topic>Analysis</topic><topic>Autophagy</topic><topic>Biochemistry & Molecular Biology</topic><topic>Cancer</topic><topic>cancer stem cell</topic><topic>Development and progression</topic><topic>Fis1</topic><topic>Genes</topic><topic>Genomes</topic><topic>Humans</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Life Sciences & Biomedicine</topic><topic>Lung</topic><topic>Lung cancer</topic><topic>Membrane Proteins</topic><topic>Metastasis</topic><topic>Mitochondria</topic><topic>Mitochondrial Dynamics - genetics</topic><topic>mitochondrial fission</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitophagy</topic><topic>Neoplasms</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Phagocytosis</topic><topic>Science & Technology</topic><topic>Stem cell research</topic><topic>Stem cells</topic><topic>stemness</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Doudou</creatorcontrib><creatorcontrib>Sun, Zhiwei</creatorcontrib><creatorcontrib>Ye, Ting</creatorcontrib><creatorcontrib>Li, Jingyuan</creatorcontrib><creatorcontrib>Zeng, Bin</creatorcontrib><creatorcontrib>Zhao, Qiting</creatorcontrib><creatorcontrib>Wang, Jianyu</creatorcontrib><creatorcontrib>Xing, Hongmei Rosie</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological 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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>FEBS open bio</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Doudou</au><au>Sun, Zhiwei</au><au>Ye, Ting</au><au>Li, Jingyuan</au><au>Zeng, Bin</au><au>Zhao, Qiting</au><au>Wang, Jianyu</au><au>Xing, Hongmei Rosie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The mitochondrial fission factor FIS1 promotes stemness of human lung cancer stem cells via mitophagy</atitle><jtitle>FEBS open bio</jtitle><stitle>FEBS OPEN BIO</stitle><addtitle>FEBS Open Bio</addtitle><date>2021-07</date><risdate>2021</risdate><volume>11</volume><issue>7</issue><spage>1997</spage><epage>2007</epage><pages>1997-2007</pages><issn>2211-5463</issn><eissn>2211-5463</eissn><abstract>Mitophagy, a form of autophagy, plays a role in cancer development, progression and recurrence. Cancer stem cells (CSCs) also play a key role in these processes, although it not known whether mitophagy can regulate the stemness of CSCs. Here, we employed the A549‐SD human non‐small cell lung adenocarcinoma CSC model that we have developed and characterized to investigate the effect of mitophagy on the stemness of CSCs. We observed a positive relationship between mitophagic activity and the stemness of lung CSCs. At the mechanistic level, our results suggest that augmentation of mitophagy in lung CSCs can be induced by FIS1 through mitochondrial fission. In addition, we assessed the clinical relevance of FIS1 in lung adenocarcinoma using The Cancer Genome Atlas database. An elevation in FIS1, when observed together with other prognostic markers for lung cancer progression, was found to correlate with shorter overall survival.
In the human non‐small cell lung adenocarcinoma cancer stem cell model A549‐SD, inhibiting the expression of FIS1 can inhibit mitochondrial division, thereby inhibiting mitophagy and consequently inhibiting the stemness of cancer stem cells.</abstract><cop>HOBOKEN</cop><pub>Wiley</pub><pmid>34051059</pmid><doi>10.1002/2211-5463.13207</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma Analysis Autophagy Biochemistry & Molecular Biology Cancer cancer stem cell Development and progression Fis1 Genes Genomes Humans Kinases Leukemia Life Sciences & Biomedicine Lung Lung cancer Membrane Proteins Metastasis Mitochondria Mitochondrial Dynamics - genetics mitochondrial fission Mitochondrial Proteins - genetics Mitophagy Neoplasms Neoplastic Stem Cells - pathology Phagocytosis Science & Technology Stem cell research Stem cells stemness Tumorigenesis Tumors Variance analysis |
| title | The mitochondrial fission factor FIS1 promotes stemness of human lung cancer stem cells via mitophagy |
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