Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway
Background Recent studies suggested that NDUFS1 has an important role in human cancers; however, the effects of NDUFS1 on gastric cancer (GC) are still not fully understood. Methods We confirmed that NDUFS1 is downregulated in GC cells through western blot immunohistochemistry and bioinformation ana...
Gespeichert in:
| Veröffentlicht in: | British journal of cancer 2023-10, Vol.129 (8), p.1261-1273 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1273 |
|---|---|
| container_issue | 8 |
| container_start_page | 1261 |
| container_title | British journal of cancer |
| container_volume | 129 |
| creator | Chen, Tao Li, Dongbao Wang, Yunliang Shen, Xiaochun Dong, Anqi Dong, Chao Duan, Kaipeng Ren, Jiayu Li, Weikang Shu, Gege Yang, Jiaoyang Xie, Yufeng Qian, Fuliang Zhou, Jin |
| description | Background
Recent studies suggested that NDUFS1 has an important role in human cancers; however, the effects of NDUFS1 on gastric cancer (GC) are still not fully understood.
Methods
We confirmed that NDUFS1 is downregulated in GC cells through western blot immunohistochemistry and bioinformation analysis. The effect of NDUFS1 on GC was studied by CCK-8, colony formation, transwell assay in vitro and Mouse xenograft assay in vivo. Expression and subcellular localization of NDUFS1 and the content of mitochondrial reactive oxygen species (mROS) was observed by confocal reflectance microscopy.
Results
Reduced expression of NDUFS1 was found in GC tissues and cell lines. Also, NDUFS1 overexpression inhibited GC cell proliferation, migration, and invasion in vitro as well as growth and metastasis in vivo. Mechanistically, NDUFS1 reduction led to the activation of the mROS-hypoxia-inducible factor 1α (HIF1α) signaling pathway. We further clarified that NDUFS1 reduction upregulated the expression of fibulin 5 (FBLN5), a transcriptional target of HIF1α, through activation of mROS-HIF1α signaling in GC cells.
Conclusions
The results of this study indicate that NDUFS1 downregulation promotes GC progression by activating an mROS-HIF1α-FBLN5 signaling pathway. |
| doi_str_mv | 10.1038/s41416-023-02409-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10575981</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2876774672</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3675-eefcc5de9a4f8e628a265a762069cd40af796d1a0a6446d431374dafa39ee4ad3</originalsourceid><addsrcrecordid>eNp9kc1u1DAUhS1ERaeFF2BliQ2bFP_bWSFoGVpp1EqUrq1bx8m4SuLBTormsfoifSY8TAWiCxZX1rW_c3SvD0JvKTmhhJsPWVBBVUUYLyVIXckXaEElZxU1TL9EC0KIrkjNyCE6yvmutDUx-hU65FqJImALNK9izji2-PLsZnlN8SbFIU4-4w7ylILDDkbn0-6-Sz7nEEd8u8XgpnAPUxg7PK09HsIU3TqOTQrQ429X19X5xZI-PlTLz6tLiXPoRuh38Aam9U_YvkYHLfTZv3k6j9HN8sv30_NqdfX14vTTqnJcaVl53zonG1-DaI1XzABTErRiRNWuEQRaXauGAoGyjmoEp1yLBlrgtfcCGn6MPu59N_Pt4BvnxylBbzcpDJC2NkKw_76MYW27eG8pkVrWhhaH908OKf6YfZ7sELLzfQ-jj3O2zEhTG6WIKei7Z-hdnFNZfEdppbVQmhWK7SmXys8n3_6ZhhK7i9XuY7UlVvs7ViuLiO9FucBj59Nf6_-ofgGqo6WT</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2876774672</pqid></control><display><type>article</type><title>Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway</title><source>SpringerLink Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Chen, Tao ; Li, Dongbao ; Wang, Yunliang ; Shen, Xiaochun ; Dong, Anqi ; Dong, Chao ; Duan, Kaipeng ; Ren, Jiayu ; Li, Weikang ; Shu, Gege ; Yang, Jiaoyang ; Xie, Yufeng ; Qian, Fuliang ; Zhou, Jin</creator><creatorcontrib>Chen, Tao ; Li, Dongbao ; Wang, Yunliang ; Shen, Xiaochun ; Dong, Anqi ; Dong, Chao ; Duan, Kaipeng ; Ren, Jiayu ; Li, Weikang ; Shu, Gege ; Yang, Jiaoyang ; Xie, Yufeng ; Qian, Fuliang ; Zhou, Jin</creatorcontrib><description>Background
Recent studies suggested that NDUFS1 has an important role in human cancers; however, the effects of NDUFS1 on gastric cancer (GC) are still not fully understood.
Methods
We confirmed that NDUFS1 is downregulated in GC cells through western blot immunohistochemistry and bioinformation analysis. The effect of NDUFS1 on GC was studied by CCK-8, colony formation, transwell assay in vitro and Mouse xenograft assay in vivo. Expression and subcellular localization of NDUFS1 and the content of mitochondrial reactive oxygen species (mROS) was observed by confocal reflectance microscopy.
Results
Reduced expression of NDUFS1 was found in GC tissues and cell lines. Also, NDUFS1 overexpression inhibited GC cell proliferation, migration, and invasion in vitro as well as growth and metastasis in vivo. Mechanistically, NDUFS1 reduction led to the activation of the mROS-hypoxia-inducible factor 1α (HIF1α) signaling pathway. We further clarified that NDUFS1 reduction upregulated the expression of fibulin 5 (FBLN5), a transcriptional target of HIF1α, through activation of mROS-HIF1α signaling in GC cells.
Conclusions
The results of this study indicate that NDUFS1 downregulation promotes GC progression by activating an mROS-HIF1α-FBLN5 signaling pathway.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/s41416-023-02409-5</identifier><identifier>PMID: 37644092</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1504/1829 ; 692/4028/67/1504/1829 ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell migration ; Cell proliferation ; Cholecystokinin ; Down-regulation ; Drug Resistance ; Epidemiology ; Gastric cancer ; Hypoxia-inducible factor 1a ; Hypoxia-inducible factors ; Immunohistochemistry ; Localization ; Metastases ; Molecular Medicine ; Oncology ; Reactive oxygen species ; Signal transduction</subject><ispartof>British journal of cancer, 2023-10, Vol.129 (8), p.1261-1273</ispartof><rights>The Author(s) 2023</rights><rights>The Author(s) 2023. 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>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3675-eefcc5de9a4f8e628a265a762069cd40af796d1a0a6446d431374dafa39ee4ad3</citedby><cites>FETCH-LOGICAL-c3675-eefcc5de9a4f8e628a265a762069cd40af796d1a0a6446d431374dafa39ee4ad3</cites><orcidid>0000-0002-1253-7951 ; 0000-0002-1244-6048 ; 0000-0002-6829-6149 ; 0000-0003-0171-9458</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/PMC10575981/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10575981/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids></links><search><creatorcontrib>Chen, Tao</creatorcontrib><creatorcontrib>Li, Dongbao</creatorcontrib><creatorcontrib>Wang, Yunliang</creatorcontrib><creatorcontrib>Shen, Xiaochun</creatorcontrib><creatorcontrib>Dong, Anqi</creatorcontrib><creatorcontrib>Dong, Chao</creatorcontrib><creatorcontrib>Duan, Kaipeng</creatorcontrib><creatorcontrib>Ren, Jiayu</creatorcontrib><creatorcontrib>Li, Weikang</creatorcontrib><creatorcontrib>Shu, Gege</creatorcontrib><creatorcontrib>Yang, Jiaoyang</creatorcontrib><creatorcontrib>Xie, Yufeng</creatorcontrib><creatorcontrib>Qian, Fuliang</creatorcontrib><creatorcontrib>Zhou, Jin</creatorcontrib><title>Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><description>Background
Recent studies suggested that NDUFS1 has an important role in human cancers; however, the effects of NDUFS1 on gastric cancer (GC) are still not fully understood.
Methods
We confirmed that NDUFS1 is downregulated in GC cells through western blot immunohistochemistry and bioinformation analysis. The effect of NDUFS1 on GC was studied by CCK-8, colony formation, transwell assay in vitro and Mouse xenograft assay in vivo. Expression and subcellular localization of NDUFS1 and the content of mitochondrial reactive oxygen species (mROS) was observed by confocal reflectance microscopy.
Results
Reduced expression of NDUFS1 was found in GC tissues and cell lines. Also, NDUFS1 overexpression inhibited GC cell proliferation, migration, and invasion in vitro as well as growth and metastasis in vivo. Mechanistically, NDUFS1 reduction led to the activation of the mROS-hypoxia-inducible factor 1α (HIF1α) signaling pathway. We further clarified that NDUFS1 reduction upregulated the expression of fibulin 5 (FBLN5), a transcriptional target of HIF1α, through activation of mROS-HIF1α signaling in GC cells.
Conclusions
The results of this study indicate that NDUFS1 downregulation promotes GC progression by activating an mROS-HIF1α-FBLN5 signaling pathway.</description><subject>631/67/1504/1829</subject><subject>692/4028/67/1504/1829</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cholecystokinin</subject><subject>Down-regulation</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Gastric cancer</subject><subject>Hypoxia-inducible factor 1a</subject><subject>Hypoxia-inducible factors</subject><subject>Immunohistochemistry</subject><subject>Localization</subject><subject>Metastases</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Reactive oxygen species</subject><subject>Signal transduction</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1u1DAUhS1ERaeFF2BliQ2bFP_bWSFoGVpp1EqUrq1bx8m4SuLBTormsfoifSY8TAWiCxZX1rW_c3SvD0JvKTmhhJsPWVBBVUUYLyVIXckXaEElZxU1TL9EC0KIrkjNyCE6yvmutDUx-hU65FqJImALNK9izji2-PLsZnlN8SbFIU4-4w7ylILDDkbn0-6-Sz7nEEd8u8XgpnAPUxg7PK09HsIU3TqOTQrQ429X19X5xZI-PlTLz6tLiXPoRuh38Aam9U_YvkYHLfTZv3k6j9HN8sv30_NqdfX14vTTqnJcaVl53zonG1-DaI1XzABTErRiRNWuEQRaXauGAoGyjmoEp1yLBlrgtfcCGn6MPu59N_Pt4BvnxylBbzcpDJC2NkKw_76MYW27eG8pkVrWhhaH908OKf6YfZ7sELLzfQ-jj3O2zEhTG6WIKei7Z-hdnFNZfEdppbVQmhWK7SmXys8n3_6ZhhK7i9XuY7UlVvs7ViuLiO9FucBj59Nf6_-ofgGqo6WT</recordid><startdate>20231012</startdate><enddate>20231012</enddate><creator>Chen, Tao</creator><creator>Li, Dongbao</creator><creator>Wang, Yunliang</creator><creator>Shen, Xiaochun</creator><creator>Dong, Anqi</creator><creator>Dong, Chao</creator><creator>Duan, Kaipeng</creator><creator>Ren, Jiayu</creator><creator>Li, Weikang</creator><creator>Shu, Gege</creator><creator>Yang, Jiaoyang</creator><creator>Xie, Yufeng</creator><creator>Qian, Fuliang</creator><creator>Zhou, Jin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1253-7951</orcidid><orcidid>https://orcid.org/0000-0002-1244-6048</orcidid><orcidid>https://orcid.org/0000-0002-6829-6149</orcidid><orcidid>https://orcid.org/0000-0003-0171-9458</orcidid></search><sort><creationdate>20231012</creationdate><title>Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway</title><author>Chen, Tao ; Li, Dongbao ; Wang, Yunliang ; Shen, Xiaochun ; Dong, Anqi ; Dong, Chao ; Duan, Kaipeng ; Ren, Jiayu ; Li, Weikang ; Shu, Gege ; Yang, Jiaoyang ; Xie, Yufeng ; Qian, Fuliang ; Zhou, Jin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3675-eefcc5de9a4f8e628a265a762069cd40af796d1a0a6446d431374dafa39ee4ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>631/67/1504/1829</topic><topic>692/4028/67/1504/1829</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cholecystokinin</topic><topic>Down-regulation</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Gastric cancer</topic><topic>Hypoxia-inducible factor 1a</topic><topic>Hypoxia-inducible factors</topic><topic>Immunohistochemistry</topic><topic>Localization</topic><topic>Metastases</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Reactive oxygen species</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Tao</creatorcontrib><creatorcontrib>Li, Dongbao</creatorcontrib><creatorcontrib>Wang, Yunliang</creatorcontrib><creatorcontrib>Shen, Xiaochun</creatorcontrib><creatorcontrib>Dong, Anqi</creatorcontrib><creatorcontrib>Dong, Chao</creatorcontrib><creatorcontrib>Duan, Kaipeng</creatorcontrib><creatorcontrib>Ren, Jiayu</creatorcontrib><creatorcontrib>Li, Weikang</creatorcontrib><creatorcontrib>Shu, Gege</creatorcontrib><creatorcontrib>Yang, Jiaoyang</creatorcontrib><creatorcontrib>Xie, Yufeng</creatorcontrib><creatorcontrib>Qian, Fuliang</creatorcontrib><creatorcontrib>Zhou, Jin</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors 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>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech 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>British Nursing Database</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>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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Tao</au><au>Li, Dongbao</au><au>Wang, Yunliang</au><au>Shen, Xiaochun</au><au>Dong, Anqi</au><au>Dong, Chao</au><au>Duan, Kaipeng</au><au>Ren, Jiayu</au><au>Li, Weikang</au><au>Shu, Gege</au><au>Yang, Jiaoyang</au><au>Xie, Yufeng</au><au>Qian, Fuliang</au><au>Zhou, Jin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><date>2023-10-12</date><risdate>2023</risdate><volume>129</volume><issue>8</issue><spage>1261</spage><epage>1273</epage><pages>1261-1273</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><abstract>Background
Recent studies suggested that NDUFS1 has an important role in human cancers; however, the effects of NDUFS1 on gastric cancer (GC) are still not fully understood.
Methods
We confirmed that NDUFS1 is downregulated in GC cells through western blot immunohistochemistry and bioinformation analysis. The effect of NDUFS1 on GC was studied by CCK-8, colony formation, transwell assay in vitro and Mouse xenograft assay in vivo. Expression and subcellular localization of NDUFS1 and the content of mitochondrial reactive oxygen species (mROS) was observed by confocal reflectance microscopy.
Results
Reduced expression of NDUFS1 was found in GC tissues and cell lines. Also, NDUFS1 overexpression inhibited GC cell proliferation, migration, and invasion in vitro as well as growth and metastasis in vivo. Mechanistically, NDUFS1 reduction led to the activation of the mROS-hypoxia-inducible factor 1α (HIF1α) signaling pathway. We further clarified that NDUFS1 reduction upregulated the expression of fibulin 5 (FBLN5), a transcriptional target of HIF1α, through activation of mROS-HIF1α signaling in GC cells.
Conclusions
The results of this study indicate that NDUFS1 downregulation promotes GC progression by activating an mROS-HIF1α-FBLN5 signaling pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>37644092</pmid><doi>10.1038/s41416-023-02409-5</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-1253-7951</orcidid><orcidid>https://orcid.org/0000-0002-1244-6048</orcidid><orcidid>https://orcid.org/0000-0002-6829-6149</orcidid><orcidid>https://orcid.org/0000-0003-0171-9458</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-0920 |
| ispartof | British journal of cancer, 2023-10, Vol.129 (8), p.1261-1273 |
| issn | 0007-0920 1532-1827 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10575981 |
| source | SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | 631/67/1504/1829 692/4028/67/1504/1829 Biomedical and Life Sciences Biomedicine Cancer Research Cell migration Cell proliferation Cholecystokinin Down-regulation Drug Resistance Epidemiology Gastric cancer Hypoxia-inducible factor 1a Hypoxia-inducible factors Immunohistochemistry Localization Metastases Molecular Medicine Oncology Reactive oxygen species Signal transduction |
| title | Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T08%3A24%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Loss%20of%20NDUFS1%20promotes%20gastric%20cancer%20progression%20by%20activating%20the%20mitochondrial%20ROS-HIF1%CE%B1-FBLN5%20signaling%20pathway&rft.jtitle=British%20journal%20of%20cancer&rft.au=Chen,%20Tao&rft.date=2023-10-12&rft.volume=129&rft.issue=8&rft.spage=1261&rft.epage=1273&rft.pages=1261-1273&rft.issn=0007-0920&rft.eissn=1532-1827&rft_id=info:doi/10.1038/s41416-023-02409-5&rft_dat=%3Cproquest_pubme%3E2876774672%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2876774672&rft_id=info:pmid/37644092&rfr_iscdi=true |