Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells
As the end product of the bacterial fermentation of dietary fiber in the colonic lumen, sodium butyrate (NaBt) has been reported to exert antitumor effects on colorectal cancer (CRC). In addition to functioning as a histone deacetylase (HDAC) inhibitor, NaBt also regulates the expression of microRNA...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2016-01, Vol.39 (5), p.1919-1929 |
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| creator | Han, Ruirui Sun, Qianqian Wu, Jianbo Zheng, Pengyuan Zhao, Guoqiang |
| description | As the end product of the bacterial fermentation of dietary fiber in the colonic lumen, sodium butyrate (NaBt) has been reported to exert antitumor effects on colorectal cancer (CRC). In addition to functioning as a histone deacetylase (HDAC) inhibitor, NaBt also regulates the expression of microRNAs (miRNAs) to inhibit CRC cell proliferation. Yet, the mechanisms involved are not completely understood. Here we investigate whether NaBt regulates miR-203 to inhibit CRC growth and explore the promising target gene of miR-203 in CRC cells.
We conducted qRT-PCR and Western blotting assays to evaluate the effects of NaBt on the expression of miR-203 and NEDD9 in HT-29 and Caco-2 cell lines. The promising target gene of miR-203 was predicted by miRNA target prediction and dual luciferase reporter assay. CRC Cell proliferation, colony formation, cell apoptosis and cell invasion assays were performed to explore the effect of NaBt, miR-203 and NEDD9 on HT-29 and Caco-2 cell lines.
The results showed that NaBt increased the expression of miR-203 to induce CRC cell apoptosis as well as inhibit cell proliferation, colony formation and cell invasion. Moreover, we determined that the NEDD9 was a target gene of miR-203. NEDD9 partially overcame the inhibitory effects of miR-203 on CRC cell colony formation and invasion.
NaBt could induce CRC cell apoptosis, inhibit CRC cell proliferation, colony formation and invasion through miR-203/NEDD9 cascade. The present study may enrich the mechanisms underlying the process that NaBt exerts anti-tumor effects on CRC cells. |
| doi_str_mv | 10.1159/000447889 |
| format | Article |
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We conducted qRT-PCR and Western blotting assays to evaluate the effects of NaBt on the expression of miR-203 and NEDD9 in HT-29 and Caco-2 cell lines. The promising target gene of miR-203 was predicted by miRNA target prediction and dual luciferase reporter assay. CRC Cell proliferation, colony formation, cell apoptosis and cell invasion assays were performed to explore the effect of NaBt, miR-203 and NEDD9 on HT-29 and Caco-2 cell lines.
The results showed that NaBt increased the expression of miR-203 to induce CRC cell apoptosis as well as inhibit cell proliferation, colony formation and cell invasion. Moreover, we determined that the NEDD9 was a target gene of miR-203. NEDD9 partially overcame the inhibitory effects of miR-203 on CRC cell colony formation and invasion.
NaBt could induce CRC cell apoptosis, inhibit CRC cell proliferation, colony formation and invasion through miR-203/NEDD9 cascade. The present study may enrich the mechanisms underlying the process that NaBt exerts anti-tumor effects on CRC cells.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000447889</identifier><identifier>PMID: 27771718</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Antibodies ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Biochemistry ; Butyric Acid - pharmacology ; Caco-2 Cells ; Cell cycle ; Cell growth ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Colorectal cancer ; Dietary fiber ; Dose-Response Relationship, Drug ; Gastroenterology ; Gene Expression Regulation, Neoplastic ; Genes ; Genes, Reporter ; HT29 Cells ; Humans ; Luciferases - genetics ; Luciferases - metabolism ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-203 ; NEDD9 ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Physiology ; Retracted Paper ; Signal Transduction ; Sodium ; Sodium butyrate</subject><ispartof>Cellular physiology and biochemistry, 2016-01, Vol.39 (5), p.1919-1929</ispartof><rights>2016 S. Karger AG, Basel</rights><rights>2016 S. Karger AG, Basel.</rights><rights>2016 S. Karger AG, Basel. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-42e4f5c54049eff96fd168f218ee381020521cbe8bcf8db830e8a6b1fc5911613</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27614,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27771718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Ruirui</creatorcontrib><creatorcontrib>Sun, Qianqian</creatorcontrib><creatorcontrib>Wu, Jianbo</creatorcontrib><creatorcontrib>Zheng, Pengyuan</creatorcontrib><creatorcontrib>Zhao, Guoqiang</creatorcontrib><title>Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>As the end product of the bacterial fermentation of dietary fiber in the colonic lumen, sodium butyrate (NaBt) has been reported to exert antitumor effects on colorectal cancer (CRC). In addition to functioning as a histone deacetylase (HDAC) inhibitor, NaBt also regulates the expression of microRNAs (miRNAs) to inhibit CRC cell proliferation. Yet, the mechanisms involved are not completely understood. Here we investigate whether NaBt regulates miR-203 to inhibit CRC growth and explore the promising target gene of miR-203 in CRC cells.
We conducted qRT-PCR and Western blotting assays to evaluate the effects of NaBt on the expression of miR-203 and NEDD9 in HT-29 and Caco-2 cell lines. The promising target gene of miR-203 was predicted by miRNA target prediction and dual luciferase reporter assay. CRC Cell proliferation, colony formation, cell apoptosis and cell invasion assays were performed to explore the effect of NaBt, miR-203 and NEDD9 on HT-29 and Caco-2 cell lines.
The results showed that NaBt increased the expression of miR-203 to induce CRC cell apoptosis as well as inhibit cell proliferation, colony formation and cell invasion. Moreover, we determined that the NEDD9 was a target gene of miR-203. NEDD9 partially overcame the inhibitory effects of miR-203 on CRC cell colony formation and invasion.
NaBt could induce CRC cell apoptosis, inhibit CRC cell proliferation, colony formation and invasion through miR-203/NEDD9 cascade. The present study may enrich the mechanisms underlying the process that NaBt exerts anti-tumor effects on CRC cells.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Antibodies</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Butyric Acid - pharmacology</subject><subject>Caco-2 Cells</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Colorectal cancer</subject><subject>Dietary fiber</subject><subject>Dose-Response Relationship, Drug</subject><subject>Gastroenterology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genes, Reporter</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Luciferases - genetics</subject><subject>Luciferases - metabolism</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-203</subject><subject>NEDD9</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Physiology</subject><subject>Retracted Paper</subject><subject>Signal Transduction</subject><subject>Sodium</subject><subject>Sodium butyrate</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkc1v1DAQxS0Eoh_0wB0hS5w4BDyOHdvHNlpKpUpU0J4txxmvsmTXi51I7X-Pl122l578Zubn90YaQt4D-wIgzVfGmBBKa_OKnILgUBml9OuiGchKG61OyFnOK1ZKZfhbcsKVUqBAn5LxV-yHeU2v5ukpuQnpwzbhch6LzHQ9_Kw4q-nisTRzHuKGTrFUmCZ6uZmG6i7FcQhYPu5mixDQT7SoNo4xFe1G2rqNx0RbHMf8jrwJbsx4cXjPycO3xX37vbr9cX3TXt5WXnIzVYKjCNJLwYTBEEwTemh04KARaw2MM8nBd6g7H3Tf6Zqhdk0HwUsD0EB9Tm72vn10K7tNw9qlJxvdYP81Ylpal6bBj2gbI9EpKAkKhQRtgi-BTpkOGyHrrnh92nttU_wzY57sKs5pU9a3NdttCI3Rhfq8p3yKOScMx1Rgdncje7xRYT8eHOdujf2R_H-U58jfLi0xHYH27mpvYbd9KNSHF6lDyl8Wcp__</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Han, Ruirui</creator><creator>Sun, Qianqian</creator><creator>Wu, Jianbo</creator><creator>Zheng, Pengyuan</creator><creator>Zhao, Guoqiang</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>DOA</scope></search><sort><creationdate>20160101</creationdate><title>Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells</title><author>Han, Ruirui ; Sun, Qianqian ; Wu, Jianbo ; Zheng, Pengyuan ; Zhao, Guoqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-42e4f5c54049eff96fd168f218ee381020521cbe8bcf8db830e8a6b1fc5911613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Antibodies</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biochemistry</topic><topic>Butyric Acid - pharmacology</topic><topic>Caco-2 Cells</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Colorectal cancer</topic><topic>Dietary fiber</topic><topic>Dose-Response Relationship, Drug</topic><topic>Gastroenterology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genes, Reporter</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Luciferases - genetics</topic><topic>Luciferases - metabolism</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-203</topic><topic>NEDD9</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><topic>Physiology</topic><topic>Retracted Paper</topic><topic>Signal Transduction</topic><topic>Sodium</topic><topic>Sodium butyrate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Ruirui</creatorcontrib><creatorcontrib>Sun, Qianqian</creatorcontrib><creatorcontrib>Wu, Jianbo</creatorcontrib><creatorcontrib>Zheng, Pengyuan</creatorcontrib><creatorcontrib>Zhao, Guoqiang</creatorcontrib><collection>Karger Open Access</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Ruirui</au><au>Sun, Qianqian</au><au>Wu, Jianbo</au><au>Zheng, Pengyuan</au><au>Zhao, Guoqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>39</volume><issue>5</issue><spage>1919</spage><epage>1929</epage><pages>1919-1929</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>As the end product of the bacterial fermentation of dietary fiber in the colonic lumen, sodium butyrate (NaBt) has been reported to exert antitumor effects on colorectal cancer (CRC). In addition to functioning as a histone deacetylase (HDAC) inhibitor, NaBt also regulates the expression of microRNAs (miRNAs) to inhibit CRC cell proliferation. Yet, the mechanisms involved are not completely understood. Here we investigate whether NaBt regulates miR-203 to inhibit CRC growth and explore the promising target gene of miR-203 in CRC cells.
We conducted qRT-PCR and Western blotting assays to evaluate the effects of NaBt on the expression of miR-203 and NEDD9 in HT-29 and Caco-2 cell lines. The promising target gene of miR-203 was predicted by miRNA target prediction and dual luciferase reporter assay. CRC Cell proliferation, colony formation, cell apoptosis and cell invasion assays were performed to explore the effect of NaBt, miR-203 and NEDD9 on HT-29 and Caco-2 cell lines.
The results showed that NaBt increased the expression of miR-203 to induce CRC cell apoptosis as well as inhibit cell proliferation, colony formation and cell invasion. Moreover, we determined that the NEDD9 was a target gene of miR-203. NEDD9 partially overcame the inhibitory effects of miR-203 on CRC cell colony formation and invasion.
NaBt could induce CRC cell apoptosis, inhibit CRC cell proliferation, colony formation and invasion through miR-203/NEDD9 cascade. The present study may enrich the mechanisms underlying the process that NaBt exerts anti-tumor effects on CRC cells.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>27771718</pmid><doi>10.1159/000447889</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Antibodies Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Biochemistry Butyric Acid - pharmacology Caco-2 Cells Cell cycle Cell growth Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Colorectal cancer Dietary fiber Dose-Response Relationship, Drug Gastroenterology Gene Expression Regulation, Neoplastic Genes Genes, Reporter HT29 Cells Humans Luciferases - genetics Luciferases - metabolism MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR-203 NEDD9 Phosphoproteins - genetics Phosphoproteins - metabolism Physiology Retracted Paper Signal Transduction Sodium Sodium butyrate |
| title | Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells |
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