Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression
Objective Lung cancer (LC) remains a threatening health issue worldwide. Methyltransferase-like protein 3 (METTL3) is imperative in carcinogenesis via m6A modification of microRNAs (miRNAs). This study estimated the effect of METTL3 in LC by regulating m6A methylation-mediated pri-miR-663 processing...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2022-12, Vol.148 (12), p.3485-3499 |
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| container_title | Journal of cancer research and clinical oncology |
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| creator | Li, Shengshu Lu, Xiaoxin Zheng, Dongyang Chen, Weizong Li, Yuzhu Li, Fang |
| description | Objective
Lung cancer (LC) remains a threatening health issue worldwide. Methyltransferase-like protein 3 (METTL3) is imperative in carcinogenesis via m6A modification of microRNAs (miRNAs). This study estimated the effect of METTL3 in LC by regulating m6A methylation-mediated pri-miR-663 processing.
Methods
miR-663 expression in 4 LC cell lines and normal HBE cells was determined using RT-qPCR. A549 and PC9 LC cells selected for in vitro studies were transfected with miR-663 mimics or inhibitor. Cell viability, migration, invasion, proliferation, and apoptosis were detected by CCK-8, Transwell, EdU, and flow cytometry assays. The downstream target genes and binding sites of miR-663 were predicted via Starbase database and validated by dual-luciferase assay. LC cells were delivered with oe-METTL3/sh-METTL3. Crosslinking between METTL3 and DGCR8 was verified by co-immunoprecipitation. Levels of m6A, miR-663, and pri-miR-663 were measured by m6A dot blot assay and RT-qPCR. m6A modification of pri-miR-663 was verified by Me-RIP assay. Finally, the effects of METTL3 in vivo were ascertained by tumor xenograft in nude mice.
Results
miR-663 was upregulated in LC cells, and miR-663 overexpression promoted cell proliferation, migration, invasion, and inhibited apoptosis, but miR-663 knockdown exerted the opposite effects. miR-663 repressed SOCS6 expression. SOCS6 overexpression annulled the promotion of miR-663 on LC cell growth. METTL3 bound to DGCR8, and METTL3 silencing elevated the levels of pri-miR-663 and m6A methylation-modified pri-miR-663, and suppressed miR-663 maturation and miR-663 expression. METTL3 facilitated tumor growth in mice through the miR-663/SOCS6 axis.
Conclusion
METTL3 promotes LC progression by accelerating m6A methylation-mediated pri-miR-663 processing and repressing SOCS6. |
| doi_str_mv | 10.1007/s00432-022-04128-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2849891996</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2727078981</sourcerecordid><originalsourceid>FETCH-LOGICAL-c338t-5e21dfc2c824f8b49e672424b86004b1c9651729afeef716a8743583f7a5316b3</originalsourceid><addsrcrecordid>eNp9kc1u1DAUhS0EotPCC7BAltiwMfgn_smyGhWKVFSJwtpyPDeDS-IMdiIxL8OzcqczgMSChWVd-zvn2vcQ8kLwN4Jz-7Zy3ijJuMTVCOmYfkRW4nAklNKPyYoLK5iWwpyR81rvOdbayqfkTOmWWy74ivz8CPPX_TCXkGsPJVRgQ_oGVNE-xDSkOcxQ6bDkLY0hRyh0V6ZtgVrTlGm3pyFGGFA4J0RGc0nHB0Osp8xG2CQ02KAojaHs6Zg-MWPUwSQePFAT8oamcYckFne36ztD4cfu1OEZedKHocLz035Bvry7-ry-Zje37z-sL29YVMrNTIMUmz7K6GTTu65pwVjZyKZzBmfUidgaLaxsQw_QW2GCs43STvU2aCVMpy7I66MvPuz7AnX2Y6r4sSFkmJbqpWta14q2NYi--ge9n5aS8XVeWmm5da0TSMkjFctUa4Hen0bgBfeH9PwxPY_p-Yf0vEbRy5P10uHo_kh-x4WAOgIVr_IWyt_e_7H9BQ-SplE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2727078981</pqid></control><display><type>article</type><title>Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Li, Shengshu ; Lu, Xiaoxin ; Zheng, Dongyang ; Chen, Weizong ; Li, Yuzhu ; Li, Fang</creator><creatorcontrib>Li, Shengshu ; Lu, Xiaoxin ; Zheng, Dongyang ; Chen, Weizong ; Li, Yuzhu ; Li, Fang</creatorcontrib><description>Objective
Lung cancer (LC) remains a threatening health issue worldwide. Methyltransferase-like protein 3 (METTL3) is imperative in carcinogenesis via m6A modification of microRNAs (miRNAs). This study estimated the effect of METTL3 in LC by regulating m6A methylation-mediated pri-miR-663 processing.
Methods
miR-663 expression in 4 LC cell lines and normal HBE cells was determined using RT-qPCR. A549 and PC9 LC cells selected for in vitro studies were transfected with miR-663 mimics or inhibitor. Cell viability, migration, invasion, proliferation, and apoptosis were detected by CCK-8, Transwell, EdU, and flow cytometry assays. The downstream target genes and binding sites of miR-663 were predicted via Starbase database and validated by dual-luciferase assay. LC cells were delivered with oe-METTL3/sh-METTL3. Crosslinking between METTL3 and DGCR8 was verified by co-immunoprecipitation. Levels of m6A, miR-663, and pri-miR-663 were measured by m6A dot blot assay and RT-qPCR. m6A modification of pri-miR-663 was verified by Me-RIP assay. Finally, the effects of METTL3 in vivo were ascertained by tumor xenograft in nude mice.
Results
miR-663 was upregulated in LC cells, and miR-663 overexpression promoted cell proliferation, migration, invasion, and inhibited apoptosis, but miR-663 knockdown exerted the opposite effects. miR-663 repressed SOCS6 expression. SOCS6 overexpression annulled the promotion of miR-663 on LC cell growth. METTL3 bound to DGCR8, and METTL3 silencing elevated the levels of pri-miR-663 and m6A methylation-modified pri-miR-663, and suppressed miR-663 maturation and miR-663 expression. METTL3 facilitated tumor growth in mice through the miR-663/SOCS6 axis.
Conclusion
METTL3 promotes LC progression by accelerating m6A methylation-mediated pri-miR-663 processing and repressing SOCS6.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-022-04128-5</identifier><identifier>PMID: 35907010</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Apoptosis ; Binding sites ; Cancer Research ; Carcinogenesis ; Cell growth ; Cell migration ; Cell proliferation ; Cell viability ; Cholecystokinin ; crosslinking ; Flow cytometry ; Hematology ; Humans ; Immunoprecipitation ; Internal Medicine ; Lung cancer ; lung neoplasms ; Lung Neoplasms - genetics ; Medicine ; Medicine & Public Health ; Methylation ; Methyltransferase ; Methyltransferases - genetics ; Methyltransferases - metabolism ; Mice ; Mice, Nude ; microRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; N6-methyladenosine ; neoplasm progression ; Oncology ; Original Article – Cancer Research ; precipitin tests ; RNA-Binding Proteins - metabolism ; Sincalide - metabolism ; Suppressor of Cytokine Signaling Proteins - genetics ; Suppressor of Cytokine Signaling Proteins - metabolism ; Tumors ; Xenografts ; xenotransplantation</subject><ispartof>Journal of cancer research and clinical oncology, 2022-12, Vol.148 (12), p.3485-3499</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c338t-5e21dfc2c824f8b49e672424b86004b1c9651729afeef716a8743583f7a5316b3</citedby><cites>FETCH-LOGICAL-c338t-5e21dfc2c824f8b49e672424b86004b1c9651729afeef716a8743583f7a5316b3</cites><orcidid>0000-0002-3521-3108</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-022-04128-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-022-04128-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35907010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shengshu</creatorcontrib><creatorcontrib>Lu, Xiaoxin</creatorcontrib><creatorcontrib>Zheng, Dongyang</creatorcontrib><creatorcontrib>Chen, Weizong</creatorcontrib><creatorcontrib>Li, Yuzhu</creatorcontrib><creatorcontrib>Li, Fang</creatorcontrib><title>Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Objective
Lung cancer (LC) remains a threatening health issue worldwide. Methyltransferase-like protein 3 (METTL3) is imperative in carcinogenesis via m6A modification of microRNAs (miRNAs). This study estimated the effect of METTL3 in LC by regulating m6A methylation-mediated pri-miR-663 processing.
Methods
miR-663 expression in 4 LC cell lines and normal HBE cells was determined using RT-qPCR. A549 and PC9 LC cells selected for in vitro studies were transfected with miR-663 mimics or inhibitor. Cell viability, migration, invasion, proliferation, and apoptosis were detected by CCK-8, Transwell, EdU, and flow cytometry assays. The downstream target genes and binding sites of miR-663 were predicted via Starbase database and validated by dual-luciferase assay. LC cells were delivered with oe-METTL3/sh-METTL3. Crosslinking between METTL3 and DGCR8 was verified by co-immunoprecipitation. Levels of m6A, miR-663, and pri-miR-663 were measured by m6A dot blot assay and RT-qPCR. m6A modification of pri-miR-663 was verified by Me-RIP assay. Finally, the effects of METTL3 in vivo were ascertained by tumor xenograft in nude mice.
Results
miR-663 was upregulated in LC cells, and miR-663 overexpression promoted cell proliferation, migration, invasion, and inhibited apoptosis, but miR-663 knockdown exerted the opposite effects. miR-663 repressed SOCS6 expression. SOCS6 overexpression annulled the promotion of miR-663 on LC cell growth. METTL3 bound to DGCR8, and METTL3 silencing elevated the levels of pri-miR-663 and m6A methylation-modified pri-miR-663, and suppressed miR-663 maturation and miR-663 expression. METTL3 facilitated tumor growth in mice through the miR-663/SOCS6 axis.
Conclusion
METTL3 promotes LC progression by accelerating m6A methylation-mediated pri-miR-663 processing and repressing SOCS6.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Binding sites</subject><subject>Cancer Research</subject><subject>Carcinogenesis</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>crosslinking</subject><subject>Flow cytometry</subject><subject>Hematology</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Internal Medicine</subject><subject>Lung cancer</subject><subject>lung neoplasms</subject><subject>Lung Neoplasms - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylation</subject><subject>Methyltransferase</subject><subject>Methyltransferases - genetics</subject><subject>Methyltransferases - metabolism</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>microRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>N6-methyladenosine</subject><subject>neoplasm progression</subject><subject>Oncology</subject><subject>Original Article – Cancer Research</subject><subject>precipitin tests</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Sincalide - metabolism</subject><subject>Suppressor of Cytokine Signaling Proteins - genetics</subject><subject>Suppressor of Cytokine Signaling Proteins - metabolism</subject><subject>Tumors</subject><subject>Xenografts</subject><subject>xenotransplantation</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kc1u1DAUhS0EotPCC7BAltiwMfgn_smyGhWKVFSJwtpyPDeDS-IMdiIxL8OzcqczgMSChWVd-zvn2vcQ8kLwN4Jz-7Zy3ijJuMTVCOmYfkRW4nAklNKPyYoLK5iWwpyR81rvOdbayqfkTOmWWy74ivz8CPPX_TCXkGsPJVRgQ_oGVNE-xDSkOcxQ6bDkLY0hRyh0V6ZtgVrTlGm3pyFGGFA4J0RGc0nHB0Osp8xG2CQ02KAojaHs6Zg-MWPUwSQePFAT8oamcYckFne36ztD4cfu1OEZedKHocLz035Bvry7-ry-Zje37z-sL29YVMrNTIMUmz7K6GTTu65pwVjZyKZzBmfUidgaLaxsQw_QW2GCs43STvU2aCVMpy7I66MvPuz7AnX2Y6r4sSFkmJbqpWta14q2NYi--ge9n5aS8XVeWmm5da0TSMkjFctUa4Hen0bgBfeH9PwxPY_p-Yf0vEbRy5P10uHo_kh-x4WAOgIVr_IWyt_e_7H9BQ-SplE</recordid><startdate>20221201</startdate><enddate>20221201</enddate><creator>Li, Shengshu</creator><creator>Lu, Xiaoxin</creator><creator>Zheng, Dongyang</creator><creator>Chen, Weizong</creator><creator>Li, Yuzhu</creator><creator>Li, Fang</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-3521-3108</orcidid></search><sort><creationdate>20221201</creationdate><title>Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression</title><author>Li, Shengshu ; Lu, Xiaoxin ; Zheng, Dongyang ; Chen, Weizong ; Li, Yuzhu ; Li, Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c338t-5e21dfc2c824f8b49e672424b86004b1c9651729afeef716a8743583f7a5316b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Binding sites</topic><topic>Cancer Research</topic><topic>Carcinogenesis</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>crosslinking</topic><topic>Flow cytometry</topic><topic>Hematology</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Internal Medicine</topic><topic>Lung cancer</topic><topic>lung neoplasms</topic><topic>Lung Neoplasms - genetics</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylation</topic><topic>Methyltransferase</topic><topic>Methyltransferases - genetics</topic><topic>Methyltransferases - metabolism</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>microRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>N6-methyladenosine</topic><topic>neoplasm progression</topic><topic>Oncology</topic><topic>Original Article – Cancer Research</topic><topic>precipitin tests</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Sincalide - metabolism</topic><topic>Suppressor of Cytokine Signaling Proteins - genetics</topic><topic>Suppressor of Cytokine Signaling Proteins - metabolism</topic><topic>Tumors</topic><topic>Xenografts</topic><topic>xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shengshu</creatorcontrib><creatorcontrib>Lu, Xiaoxin</creatorcontrib><creatorcontrib>Zheng, Dongyang</creatorcontrib><creatorcontrib>Chen, Weizong</creatorcontrib><creatorcontrib>Li, Yuzhu</creatorcontrib><creatorcontrib>Li, Fang</creatorcontrib><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>Oncogenes and Growth Factors 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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shengshu</au><au>Lu, Xiaoxin</au><au>Zheng, Dongyang</au><au>Chen, Weizong</au><au>Li, Yuzhu</au><au>Li, Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2022-12-01</date><risdate>2022</risdate><volume>148</volume><issue>12</issue><spage>3485</spage><epage>3499</epage><pages>3485-3499</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Objective
Lung cancer (LC) remains a threatening health issue worldwide. Methyltransferase-like protein 3 (METTL3) is imperative in carcinogenesis via m6A modification of microRNAs (miRNAs). This study estimated the effect of METTL3 in LC by regulating m6A methylation-mediated pri-miR-663 processing.
Methods
miR-663 expression in 4 LC cell lines and normal HBE cells was determined using RT-qPCR. A549 and PC9 LC cells selected for in vitro studies were transfected with miR-663 mimics or inhibitor. Cell viability, migration, invasion, proliferation, and apoptosis were detected by CCK-8, Transwell, EdU, and flow cytometry assays. The downstream target genes and binding sites of miR-663 were predicted via Starbase database and validated by dual-luciferase assay. LC cells were delivered with oe-METTL3/sh-METTL3. Crosslinking between METTL3 and DGCR8 was verified by co-immunoprecipitation. Levels of m6A, miR-663, and pri-miR-663 were measured by m6A dot blot assay and RT-qPCR. m6A modification of pri-miR-663 was verified by Me-RIP assay. Finally, the effects of METTL3 in vivo were ascertained by tumor xenograft in nude mice.
Results
miR-663 was upregulated in LC cells, and miR-663 overexpression promoted cell proliferation, migration, invasion, and inhibited apoptosis, but miR-663 knockdown exerted the opposite effects. miR-663 repressed SOCS6 expression. SOCS6 overexpression annulled the promotion of miR-663 on LC cell growth. METTL3 bound to DGCR8, and METTL3 silencing elevated the levels of pri-miR-663 and m6A methylation-modified pri-miR-663, and suppressed miR-663 maturation and miR-663 expression. METTL3 facilitated tumor growth in mice through the miR-663/SOCS6 axis.
Conclusion
METTL3 promotes LC progression by accelerating m6A methylation-mediated pri-miR-663 processing and repressing SOCS6.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35907010</pmid><doi>10.1007/s00432-022-04128-5</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-3521-3108</orcidid></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Apoptosis Binding sites Cancer Research Carcinogenesis Cell growth Cell migration Cell proliferation Cell viability Cholecystokinin crosslinking Flow cytometry Hematology Humans Immunoprecipitation Internal Medicine Lung cancer lung neoplasms Lung Neoplasms - genetics Medicine Medicine & Public Health Methylation Methyltransferase Methyltransferases - genetics Methyltransferases - metabolism Mice Mice, Nude microRNA MicroRNAs - genetics MicroRNAs - metabolism miRNA N6-methyladenosine neoplasm progression Oncology Original Article – Cancer Research precipitin tests RNA-Binding Proteins - metabolism Sincalide - metabolism Suppressor of Cytokine Signaling Proteins - genetics Suppressor of Cytokine Signaling Proteins - metabolism Tumors Xenografts xenotransplantation |
| title | Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression |
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