Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression
Angiogenesis is a key event in non-small cell lung cancer progression. Alginic acid (AA), a kind of naturally occurring polyuronic acid, is generally enriched in edible brown algae. Recent studies have uncovered its anti-anaphylactic and anti-inflammatory properties. However, the effects of AA on hu...
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| Veröffentlicht in: | Journal of natural medicines 2021-06, Vol.75 (3), p.553-564 |
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| description | Angiogenesis is a key event in non-small cell lung cancer progression. Alginic acid (AA), a kind of naturally occurring polyuronic acid, is generally enriched in edible brown algae. Recent studies have uncovered its anti-anaphylactic and anti-inflammatory properties. However, the effects of AA on human malignancies remain unknown. Herein, efficient inhibition of AA on NSCLC-induced angiogenesis was observed with tube formation and xenograft models. Subsequent results indicated that AA downregulated the expression of VEGF-A, a key angiogenesis-inducing cytokine. In addition, AA downregulated STAT3, a transcriptional inducer of VEGF-A and increased non-coding RNA miR-506 expression, respectively. Furthermore, miR-506 directly modulated STAT3 relying on base pairing the 3′-UTR in STAT3 mRNA. We also found that abrogation of miR-506 abolished the inhibitory effect of AA on VEGF-A expression and NSCLC-induced angiogenesis. Finally, xenografts experiments also showed that oral administration of AA could significantly attenuate NSCLC angiogenesis, indicated by decreased micro-vessel density (MVD) and the MVD marker CD31 expression in xenografts tissues. Correspondingly, AA treatment also downregulated VEGF-A, STAT3 and increased miR-506 expression in xenografts samples, respectively. Taken together, these results suggested that AA could suppress NSCLC-induced angiogenesis via miR-506/STAT3/VEGF-A axis.
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| doi_str_mv | 10.1007/s11418-021-01493-2 |
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.</description><identifier>ISSN: 1340-3443</identifier><identifier>EISSN: 1861-0293</identifier><identifier>DOI: 10.1007/s11418-021-01493-2</identifier><identifier>PMID: 33666835</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>3' Untranslated regions ; A549 Cells ; Algae ; Alginic acid ; Alginic Acid - pharmacology ; Anaphylaxis ; Angiogenesis ; Animals ; Anti-inflammatory agents ; Biological products ; Biomedical and Life Sciences ; Biomedicine ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell Proliferation ; Complementary & Alternative Medicine ; Cytokines ; Down-Regulation ; Flowers & plants ; Human Umbilical Vein Endothelial Cells ; Humans ; Inflammation ; Lung cancer ; Lung Neoplasms - pathology ; Medicinal Chemistry ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neovascularization, Pathologic - drug therapy ; Non-coding RNA ; Non-small cell lung carcinoma ; Oral administration ; Original Paper ; Pharmacology/Toxicology ; Pharmacy ; Plant Sciences ; RNA, Messenger ; Signal Transduction ; Small cell lung carcinoma ; Stat3 protein ; STAT3 Transcription Factor ; Transcription ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Journal of natural medicines, 2021-06, Vol.75 (3), p.553-564</ispartof><rights>The Japanese Society of Pharmacognosy 2021</rights><rights>The Japanese Society of Pharmacognosy 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-439eb4498d4fde0a9626f5e547a1e6d18086139430233881017befea0db4629c3</citedby><cites>FETCH-LOGICAL-c426t-439eb4498d4fde0a9626f5e547a1e6d18086139430233881017befea0db4629c3</cites><orcidid>0000-0002-4485-2104</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/s11418-021-01493-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11418-021-01493-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33666835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Keping</creatorcontrib><creatorcontrib>Wang, Bin</creatorcontrib><creatorcontrib>Wang, Zunqiao</creatorcontrib><creatorcontrib>Yang, Rusong</creatorcontrib><title>Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression</title><title>Journal of natural medicines</title><addtitle>J Nat Med</addtitle><addtitle>J Nat Med</addtitle><description>Angiogenesis is a key event in non-small cell lung cancer progression. Alginic acid (AA), a kind of naturally occurring polyuronic acid, is generally enriched in edible brown algae. Recent studies have uncovered its anti-anaphylactic and anti-inflammatory properties. However, the effects of AA on human malignancies remain unknown. Herein, efficient inhibition of AA on NSCLC-induced angiogenesis was observed with tube formation and xenograft models. Subsequent results indicated that AA downregulated the expression of VEGF-A, a key angiogenesis-inducing cytokine. In addition, AA downregulated STAT3, a transcriptional inducer of VEGF-A and increased non-coding RNA miR-506 expression, respectively. Furthermore, miR-506 directly modulated STAT3 relying on base pairing the 3′-UTR in STAT3 mRNA. We also found that abrogation of miR-506 abolished the inhibitory effect of AA on VEGF-A expression and NSCLC-induced angiogenesis. Finally, xenografts experiments also showed that oral administration of AA could significantly attenuate NSCLC angiogenesis, indicated by decreased micro-vessel density (MVD) and the MVD marker CD31 expression in xenografts tissues. Correspondingly, AA treatment also downregulated VEGF-A, STAT3 and increased miR-506 expression in xenografts samples, respectively. Taken together, these results suggested that AA could suppress NSCLC-induced angiogenesis via miR-506/STAT3/VEGF-A axis.
.</description><subject>3' Untranslated regions</subject><subject>A549 Cells</subject><subject>Algae</subject><subject>Alginic acid</subject><subject>Alginic Acid - pharmacology</subject><subject>Anaphylaxis</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Biological products</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Complementary & Alternative Medicine</subject><subject>Cytokines</subject><subject>Down-Regulation</subject><subject>Flowers & plants</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - pathology</subject><subject>Medicinal Chemistry</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Non-coding RNA</subject><subject>Non-small cell lung carcinoma</subject><subject>Oral administration</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Pharmacy</subject><subject>Plant Sciences</subject><subject>RNA, Messenger</subject><subject>Signal Transduction</subject><subject>Small cell lung carcinoma</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor</subject><subject>Transcription</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>1340-3443</issn><issn>1861-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtP3TAQhS0E4v0HukCR2LAxjD2Ob7JECFokpEqIri3HmQSjxLnYCSr_vqYXitQFGz_kb874zGHsm4BzAbC6SEIoUXGQgoNQNXK5xfZFpfNV1ridz6iAo1K4xw5SegJQElHssj1ErXWF5T7rL4feB-8K63xb-PDoGz-nIkyBp9EOQ-EoL8MS-sLZ4ChyH9rFUVvY0Pupp0DJp-LF26ww-xc7-4yO_p6XoAv6vY6Ukp_CEdvp7JDo-H0_ZL9urh-ufvC7n99vry7vuFNSz1xhTY1SddWqriWwtZa6K6lUKytIt6KCbA9rhZCdVJUAsWqoIwtto7SsHR6ys43uOk7PC6XZjD69ebCBpiUZmbXVqpayyujpf-jTtMSQf2dkiXlEEgEyJTeUi1NKkTqzjn608dUIMG8xmE0MJsdg_sZgZC46eZdempHafyUfc88AboCUn0JP8bP3F7J_ALx9kXM</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Wang, Keping</creator><creator>Wang, Bin</creator><creator>Wang, Zunqiao</creator><creator>Yang, Rusong</creator><general>Springer Singapore</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>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4485-2104</orcidid></search><sort><creationdate>20210601</creationdate><title>Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression</title><author>Wang, Keping ; Wang, Bin ; Wang, Zunqiao ; Yang, Rusong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-439eb4498d4fde0a9626f5e547a1e6d18086139430233881017befea0db4629c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>3' Untranslated regions</topic><topic>A549 Cells</topic><topic>Algae</topic><topic>Alginic acid</topic><topic>Alginic Acid - pharmacology</topic><topic>Anaphylaxis</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Anti-inflammatory agents</topic><topic>Biological products</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Complementary & Alternative Medicine</topic><topic>Cytokines</topic><topic>Down-Regulation</topic><topic>Flowers & plants</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - pathology</topic><topic>Medicinal Chemistry</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Non-coding RNA</topic><topic>Non-small cell lung carcinoma</topic><topic>Oral administration</topic><topic>Original Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Pharmacy</topic><topic>Plant Sciences</topic><topic>RNA, Messenger</topic><topic>Signal Transduction</topic><topic>Small cell lung carcinoma</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor</topic><topic>Transcription</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Keping</creatorcontrib><creatorcontrib>Wang, Bin</creatorcontrib><creatorcontrib>Wang, Zunqiao</creatorcontrib><creatorcontrib>Yang, Rusong</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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of natural medicines</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Keping</au><au>Wang, Bin</au><au>Wang, Zunqiao</au><au>Yang, Rusong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression</atitle><jtitle>Journal of natural medicines</jtitle><stitle>J Nat Med</stitle><addtitle>J Nat Med</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>75</volume><issue>3</issue><spage>553</spage><epage>564</epage><pages>553-564</pages><issn>1340-3443</issn><eissn>1861-0293</eissn><abstract>Angiogenesis is a key event in non-small cell lung cancer progression. Alginic acid (AA), a kind of naturally occurring polyuronic acid, is generally enriched in edible brown algae. Recent studies have uncovered its anti-anaphylactic and anti-inflammatory properties. However, the effects of AA on human malignancies remain unknown. Herein, efficient inhibition of AA on NSCLC-induced angiogenesis was observed with tube formation and xenograft models. Subsequent results indicated that AA downregulated the expression of VEGF-A, a key angiogenesis-inducing cytokine. In addition, AA downregulated STAT3, a transcriptional inducer of VEGF-A and increased non-coding RNA miR-506 expression, respectively. Furthermore, miR-506 directly modulated STAT3 relying on base pairing the 3′-UTR in STAT3 mRNA. We also found that abrogation of miR-506 abolished the inhibitory effect of AA on VEGF-A expression and NSCLC-induced angiogenesis. Finally, xenografts experiments also showed that oral administration of AA could significantly attenuate NSCLC angiogenesis, indicated by decreased micro-vessel density (MVD) and the MVD marker CD31 expression in xenografts tissues. Correspondingly, AA treatment also downregulated VEGF-A, STAT3 and increased miR-506 expression in xenografts samples, respectively. Taken together, these results suggested that AA could suppress NSCLC-induced angiogenesis via miR-506/STAT3/VEGF-A axis.
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| subjects | 3' Untranslated regions A549 Cells Algae Alginic acid Alginic Acid - pharmacology Anaphylaxis Angiogenesis Animals Anti-inflammatory agents Biological products Biomedical and Life Sciences Biomedicine Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Proliferation Complementary & Alternative Medicine Cytokines Down-Regulation Flowers & plants Human Umbilical Vein Endothelial Cells Humans Inflammation Lung cancer Lung Neoplasms - pathology Medicinal Chemistry Mice Mice, Inbred BALB C Mice, Nude MicroRNAs - genetics MicroRNAs - metabolism Neovascularization, Pathologic - drug therapy Non-coding RNA Non-small cell lung carcinoma Oral administration Original Paper Pharmacology/Toxicology Pharmacy Plant Sciences RNA, Messenger Signal Transduction Small cell lung carcinoma Stat3 protein STAT3 Transcription Factor Transcription Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism Xenograft Model Antitumor Assays Xenografts |
| title | Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression |
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