RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner
Background Having emerged as the most abundant posttranscriptional internal mRNA modification in eukaryotes, N6‐methyladenosine (m6A) has attracted tremendous scientific interest in recent years. However, the functional importance of the m6A methylation machinery in ferroptosis regulation in hypopha...
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description | Background
Having emerged as the most abundant posttranscriptional internal mRNA modification in eukaryotes, N6‐methyladenosine (m6A) has attracted tremendous scientific interest in recent years. However, the functional importance of the m6A methylation machinery in ferroptosis regulation in hypopharyngeal squamous cell carcinoma (HPSCC) remains unclear.
Methods
We herein performed bioinformatic analysis, cell biological analyses, transcriptome‐wide m6A sequencing (m6A‐seq, MeRIP‐seq), RNA sequencing (RNA‐seq), and RNA immunoprecipitation sequencing (RIP‐seq), followed by m6A dot blot, MeRIP‐qPCR, RIP‐qPCR, and dual‐luciferase reporter assays.
Results
The results revealed that ALKBH5‐mediated m6A demethylation led to the posttranscriptional inhibition of NFE2L2/NRF2, which is crucial for the regulation of antioxidant molecules in cells, at two m6A residues in the 3′‐UTR. Knocking down ALKBH5 subsequently increased the expression of NFE2L2/NRF2 and increased the resistance of HPSCC cells to ferroptosis. In addition, m6A‐mediated NFE2L2/NRF2 stabilization was dependent on the m6A reader IGF2BP2. We suggest that ALKBH5 dysregulates NFE2L2/NRF2 expression in HPSCC through an m6A‐IGF2BP2‐dependent mechanism.
Conclusion
Together, these results have revealed an association between the ALKBH5‐NFE2L2/NRF2 axis and ferroptosis, providing insight into the functional importance of reversible mRNA m6A methylation and its modulators in HPSCC.
RSL3‐induced head and neck cancer cell ferroptosis is closely correlated with the global m6A abundance. (a, b) Cell viability (a) and LDH release assays (b) of HNSCC cell lines that had been exposed to different concentrations of RSL3 for 24 h. (c) Measurement of cellular lipid ROS levels by BODIPY C11 staining after exposure to RSL3 for 24 h. (d) Western blot analysis of Detroit 562 and SCC25 cells exposed to various concentrations of RSL3 for 24 h. β‐Actin was used as the loading control. (e, f) Representative images of the m6A dot blot assay (e) and quantitation of m6A (f) showing the global m6A abundance in HNSCC cells. MB, methylene blue staining (as a loading control). (g) Heat map of HNSCC cells with hierarchical clustering of ferroptosis‐sensitive and ferroptosis‐insensitive cells; each value was normalized to the corresponding mean value. |
doi_str_mv | 10.1002/jcla.24514 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9279968</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2688887124</sourcerecordid><originalsourceid>FETCH-LOGICAL-p1614-4c2626e2a73f91a9b0fced3738f3654d530c0d41f2fdc92985a1ea7f467200913</originalsourceid><addsrcrecordid>eNpVkc1u1DAUhSMEokNhwxNYYp3WP4ljb5DSUactRAOqYG3dcZwZjxw7tZOi7HgEnoPH4klIf4TE3dwj3aNPV-dk2XuCzwjG9PyoHZzRoiTFi2xFsBQ5FbR8ma2wEFUuMGEn2ZuUjhhjIQl_nZ2wkgtZsmqV_b7d1qg1vRkPs4NkUN18vrguUTT7ycFoEjrMQxgOEGe_N-BQupugD1NC2jiHNERtfegBdSbGMIwh2YR2MxpCGscIPuloh9EGD87NCPRo72G0fo-2m0va0PPt7YYi6xF41PP6z89fN1cbevGVLqo1g_Gt8SPqwXsT32avOnDJvHvep9n3zeW39XXefLm6WddNPhBOirzQlFNuKFSskwTkDnfatKxiomO8LNqSYY3bgnS0a7WkUpRADFRdwSuKsSTsNPv4xB2mXW9avXwQwakh2n5JQQWw6v-Ltwe1D_dK0kpKLhbAh2dADHeTSaM6hikuCSRFuVimIrRYXOTJ9cM6M__DE6weSlUPparHUtWndVM_KvYXu-Waag</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2688887124</pqid></control><display><type>article</type><title>RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner</title><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><creator>Ye, Jing ; Chen, Xiaozhen ; Jiang, Xiaohua ; Dong, Zhihuai ; Hu, Sunhong ; Xiao, Mang</creator><creatorcontrib>Ye, Jing ; Chen, Xiaozhen ; Jiang, Xiaohua ; Dong, Zhihuai ; Hu, Sunhong ; Xiao, Mang</creatorcontrib><description>Background
Having emerged as the most abundant posttranscriptional internal mRNA modification in eukaryotes, N6‐methyladenosine (m6A) has attracted tremendous scientific interest in recent years. However, the functional importance of the m6A methylation machinery in ferroptosis regulation in hypopharyngeal squamous cell carcinoma (HPSCC) remains unclear.
Methods
We herein performed bioinformatic analysis, cell biological analyses, transcriptome‐wide m6A sequencing (m6A‐seq, MeRIP‐seq), RNA sequencing (RNA‐seq), and RNA immunoprecipitation sequencing (RIP‐seq), followed by m6A dot blot, MeRIP‐qPCR, RIP‐qPCR, and dual‐luciferase reporter assays.
Results
The results revealed that ALKBH5‐mediated m6A demethylation led to the posttranscriptional inhibition of NFE2L2/NRF2, which is crucial for the regulation of antioxidant molecules in cells, at two m6A residues in the 3′‐UTR. Knocking down ALKBH5 subsequently increased the expression of NFE2L2/NRF2 and increased the resistance of HPSCC cells to ferroptosis. In addition, m6A‐mediated NFE2L2/NRF2 stabilization was dependent on the m6A reader IGF2BP2. We suggest that ALKBH5 dysregulates NFE2L2/NRF2 expression in HPSCC through an m6A‐IGF2BP2‐dependent mechanism.
Conclusion
Together, these results have revealed an association between the ALKBH5‐NFE2L2/NRF2 axis and ferroptosis, providing insight into the functional importance of reversible mRNA m6A methylation and its modulators in HPSCC.
RSL3‐induced head and neck cancer cell ferroptosis is closely correlated with the global m6A abundance. (a, b) Cell viability (a) and LDH release assays (b) of HNSCC cell lines that had been exposed to different concentrations of RSL3 for 24 h. (c) Measurement of cellular lipid ROS levels by BODIPY C11 staining after exposure to RSL3 for 24 h. (d) Western blot analysis of Detroit 562 and SCC25 cells exposed to various concentrations of RSL3 for 24 h. β‐Actin was used as the loading control. (e, f) Representative images of the m6A dot blot assay (e) and quantitation of m6A (f) showing the global m6A abundance in HNSCC cells. MB, methylene blue staining (as a loading control). (g) Heat map of HNSCC cells with hierarchical clustering of ferroptosis‐sensitive and ferroptosis‐insensitive cells; each value was normalized to the corresponding mean value.</description><identifier>ISSN: 0887-8013</identifier><identifier>EISSN: 1098-2825</identifier><identifier>DOI: 10.1002/jcla.24514</identifier><identifier>PMID: 35689537</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>3' Untranslated regions ; ALKBH5 ; Antioxidants ; Apoptosis ; Autophagy ; Cancer ; Demethylation ; Ferroptosis ; HPSCC ; Immunomodulation ; Immunoprecipitation ; Laboratory animals ; Lipids ; m6A modification ; Medical research ; Methylation ; N6-methyladenosine ; NFE2L2/NRF2 ; Post-transcription ; Proteins ; RNA modification ; Squamous cell carcinoma ; Throat cancer ; Transcriptomes ; Variance analysis</subject><ispartof>Journal of clinical laboratory analysis, 2022-07, Vol.36 (7), p.n/a</ispartof><rights>2022 The Authors. published by Wiley Periodicals LLC.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by-nc-nd/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><orcidid>0000-0002-7131-6251</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/PMC9279968/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279968/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids></links><search><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Chen, Xiaozhen</creatorcontrib><creatorcontrib>Jiang, Xiaohua</creatorcontrib><creatorcontrib>Dong, Zhihuai</creatorcontrib><creatorcontrib>Hu, Sunhong</creatorcontrib><creatorcontrib>Xiao, Mang</creatorcontrib><title>RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner</title><title>Journal of clinical laboratory analysis</title><description>Background
Having emerged as the most abundant posttranscriptional internal mRNA modification in eukaryotes, N6‐methyladenosine (m6A) has attracted tremendous scientific interest in recent years. However, the functional importance of the m6A methylation machinery in ferroptosis regulation in hypopharyngeal squamous cell carcinoma (HPSCC) remains unclear.
Methods
We herein performed bioinformatic analysis, cell biological analyses, transcriptome‐wide m6A sequencing (m6A‐seq, MeRIP‐seq), RNA sequencing (RNA‐seq), and RNA immunoprecipitation sequencing (RIP‐seq), followed by m6A dot blot, MeRIP‐qPCR, RIP‐qPCR, and dual‐luciferase reporter assays.
Results
The results revealed that ALKBH5‐mediated m6A demethylation led to the posttranscriptional inhibition of NFE2L2/NRF2, which is crucial for the regulation of antioxidant molecules in cells, at two m6A residues in the 3′‐UTR. Knocking down ALKBH5 subsequently increased the expression of NFE2L2/NRF2 and increased the resistance of HPSCC cells to ferroptosis. In addition, m6A‐mediated NFE2L2/NRF2 stabilization was dependent on the m6A reader IGF2BP2. We suggest that ALKBH5 dysregulates NFE2L2/NRF2 expression in HPSCC through an m6A‐IGF2BP2‐dependent mechanism.
Conclusion
Together, these results have revealed an association between the ALKBH5‐NFE2L2/NRF2 axis and ferroptosis, providing insight into the functional importance of reversible mRNA m6A methylation and its modulators in HPSCC.
RSL3‐induced head and neck cancer cell ferroptosis is closely correlated with the global m6A abundance. (a, b) Cell viability (a) and LDH release assays (b) of HNSCC cell lines that had been exposed to different concentrations of RSL3 for 24 h. (c) Measurement of cellular lipid ROS levels by BODIPY C11 staining after exposure to RSL3 for 24 h. (d) Western blot analysis of Detroit 562 and SCC25 cells exposed to various concentrations of RSL3 for 24 h. β‐Actin was used as the loading control. (e, f) Representative images of the m6A dot blot assay (e) and quantitation of m6A (f) showing the global m6A abundance in HNSCC cells. MB, methylene blue staining (as a loading control). (g) Heat map of HNSCC cells with hierarchical clustering of ferroptosis‐sensitive and ferroptosis‐insensitive cells; each value was normalized to the corresponding mean value.</description><subject>3' Untranslated regions</subject><subject>ALKBH5</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Cancer</subject><subject>Demethylation</subject><subject>Ferroptosis</subject><subject>HPSCC</subject><subject>Immunomodulation</subject><subject>Immunoprecipitation</subject><subject>Laboratory animals</subject><subject>Lipids</subject><subject>m6A modification</subject><subject>Medical research</subject><subject>Methylation</subject><subject>N6-methyladenosine</subject><subject>NFE2L2/NRF2</subject><subject>Post-transcription</subject><subject>Proteins</subject><subject>RNA modification</subject><subject>Squamous cell carcinoma</subject><subject>Throat cancer</subject><subject>Transcriptomes</subject><subject>Variance analysis</subject><issn>0887-8013</issn><issn>1098-2825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpVkc1u1DAUhSMEokNhwxNYYp3WP4ljb5DSUactRAOqYG3dcZwZjxw7tZOi7HgEnoPH4klIf4TE3dwj3aNPV-dk2XuCzwjG9PyoHZzRoiTFi2xFsBQ5FbR8ma2wEFUuMGEn2ZuUjhhjIQl_nZ2wkgtZsmqV_b7d1qg1vRkPs4NkUN18vrguUTT7ycFoEjrMQxgOEGe_N-BQupugD1NC2jiHNERtfegBdSbGMIwh2YR2MxpCGscIPuloh9EGD87NCPRo72G0fo-2m0va0PPt7YYi6xF41PP6z89fN1cbevGVLqo1g_Gt8SPqwXsT32avOnDJvHvep9n3zeW39XXefLm6WddNPhBOirzQlFNuKFSskwTkDnfatKxiomO8LNqSYY3bgnS0a7WkUpRADFRdwSuKsSTsNPv4xB2mXW9avXwQwakh2n5JQQWw6v-Ltwe1D_dK0kpKLhbAh2dADHeTSaM6hikuCSRFuVimIrRYXOTJ9cM6M__DE6weSlUPparHUtWndVM_KvYXu-Waag</recordid><startdate>202207</startdate><enddate>202207</enddate><creator>Ye, Jing</creator><creator>Chen, Xiaozhen</creator><creator>Jiang, Xiaohua</creator><creator>Dong, Zhihuai</creator><creator>Hu, Sunhong</creator><creator>Xiao, Mang</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</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>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>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7131-6251</orcidid></search><sort><creationdate>202207</creationdate><title>RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner</title><author>Ye, Jing ; Chen, Xiaozhen ; Jiang, Xiaohua ; Dong, Zhihuai ; Hu, Sunhong ; Xiao, Mang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1614-4c2626e2a73f91a9b0fced3738f3654d530c0d41f2fdc92985a1ea7f467200913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3' Untranslated regions</topic><topic>ALKBH5</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Cancer</topic><topic>Demethylation</topic><topic>Ferroptosis</topic><topic>HPSCC</topic><topic>Immunomodulation</topic><topic>Immunoprecipitation</topic><topic>Laboratory animals</topic><topic>Lipids</topic><topic>m6A modification</topic><topic>Medical research</topic><topic>Methylation</topic><topic>N6-methyladenosine</topic><topic>NFE2L2/NRF2</topic><topic>Post-transcription</topic><topic>Proteins</topic><topic>RNA modification</topic><topic>Squamous cell carcinoma</topic><topic>Throat cancer</topic><topic>Transcriptomes</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Chen, Xiaozhen</creatorcontrib><creatorcontrib>Jiang, Xiaohua</creatorcontrib><creatorcontrib>Dong, Zhihuai</creatorcontrib><creatorcontrib>Hu, Sunhong</creatorcontrib><creatorcontrib>Xiao, Mang</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical laboratory analysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ye, Jing</au><au>Chen, Xiaozhen</au><au>Jiang, Xiaohua</au><au>Dong, Zhihuai</au><au>Hu, Sunhong</au><au>Xiao, Mang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner</atitle><jtitle>Journal of clinical laboratory analysis</jtitle><date>2022-07</date><risdate>2022</risdate><volume>36</volume><issue>7</issue><epage>n/a</epage><issn>0887-8013</issn><eissn>1098-2825</eissn><abstract>Background
Having emerged as the most abundant posttranscriptional internal mRNA modification in eukaryotes, N6‐methyladenosine (m6A) has attracted tremendous scientific interest in recent years. However, the functional importance of the m6A methylation machinery in ferroptosis regulation in hypopharyngeal squamous cell carcinoma (HPSCC) remains unclear.
Methods
We herein performed bioinformatic analysis, cell biological analyses, transcriptome‐wide m6A sequencing (m6A‐seq, MeRIP‐seq), RNA sequencing (RNA‐seq), and RNA immunoprecipitation sequencing (RIP‐seq), followed by m6A dot blot, MeRIP‐qPCR, RIP‐qPCR, and dual‐luciferase reporter assays.
Results
The results revealed that ALKBH5‐mediated m6A demethylation led to the posttranscriptional inhibition of NFE2L2/NRF2, which is crucial for the regulation of antioxidant molecules in cells, at two m6A residues in the 3′‐UTR. Knocking down ALKBH5 subsequently increased the expression of NFE2L2/NRF2 and increased the resistance of HPSCC cells to ferroptosis. In addition, m6A‐mediated NFE2L2/NRF2 stabilization was dependent on the m6A reader IGF2BP2. We suggest that ALKBH5 dysregulates NFE2L2/NRF2 expression in HPSCC through an m6A‐IGF2BP2‐dependent mechanism.
Conclusion
Together, these results have revealed an association between the ALKBH5‐NFE2L2/NRF2 axis and ferroptosis, providing insight into the functional importance of reversible mRNA m6A methylation and its modulators in HPSCC.
RSL3‐induced head and neck cancer cell ferroptosis is closely correlated with the global m6A abundance. (a, b) Cell viability (a) and LDH release assays (b) of HNSCC cell lines that had been exposed to different concentrations of RSL3 for 24 h. (c) Measurement of cellular lipid ROS levels by BODIPY C11 staining after exposure to RSL3 for 24 h. (d) Western blot analysis of Detroit 562 and SCC25 cells exposed to various concentrations of RSL3 for 24 h. β‐Actin was used as the loading control. (e, f) Representative images of the m6A dot blot assay (e) and quantitation of m6A (f) showing the global m6A abundance in HNSCC cells. MB, methylene blue staining (as a loading control). (g) Heat map of HNSCC cells with hierarchical clustering of ferroptosis‐sensitive and ferroptosis‐insensitive cells; each value was normalized to the corresponding mean value.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>35689537</pmid><doi>10.1002/jcla.24514</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-7131-6251</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated regions ALKBH5 Antioxidants Apoptosis Autophagy Cancer Demethylation Ferroptosis HPSCC Immunomodulation Immunoprecipitation Laboratory animals Lipids m6A modification Medical research Methylation N6-methyladenosine NFE2L2/NRF2 Post-transcription Proteins RNA modification Squamous cell carcinoma Throat cancer Transcriptomes Variance analysis |
title | RNA demethylase ALKBH5 regulates hypopharyngeal squamous cell carcinoma ferroptosis by posttranscriptionally activating NFE2L2/NRF2 in an m6A‐IGF2BP2‐dependent manner |
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