Circ_0007031 Silencing Inhibits Cell Proliferation and Induces Cell Apoptosis via Downregulating MELK at a miR-485-3p-Dependent Way in Colorectal Cancer
Colorectal cancer (CRC) is a malignant cancer with an increasing incidence. Circular RNA (circRNA) is recently found to participate in the regulation of CRC progression. However, the role of circ_0007031 in CRC malignant progression remains elusive. 50 CRC patients were implicated in this study. Qua...
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| Veröffentlicht in: | Biochemical genetics 2022-04, Vol.60 (2), p.576-597 |
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| creator | Su, Shengtian Lu, Wenjing Liu, Jun Li, Liping Liu, Liang Li, Xiaoju Ye, Dan Yu, Zhigao |
| description | Colorectal cancer (CRC) is a malignant cancer with an increasing incidence. Circular RNA (circRNA) is recently found to participate in the regulation of CRC progression. However, the role of circ_0007031 in CRC malignant progression remains elusive. 50 CRC patients were implicated in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the RNA expression of circ_0007031, microRNA-485-3p (miR-485-3p) and maternal embryonic leucine zipper kinase (MELK). Western blot analysis was conducted to determine protein expression. Cell viability and proliferation were demonstrated by cell counting kit-8 and 5-Ethynyl-29-deoxyuridine (EdU) assays, respectively. Cell cycle and apoptosis were investigated by flow cytometry analysis. The interaction among circ_0007031, miR-485-3p and MELK was predicted by online databases, and identified by dual-luciferase reporter assay. Mouse model assay was conducted to reveal the effect of circ_0007031 on tumor formation in vivo. Circ_0007031 and MELK expression were obviously increased, while miR-485-3p expression was decreased in CRC tissues and cells compared with normal colorectal tissues or cells. Circ_0007031 knockdown repressed proliferation, whereas induced cell arrest at G0/G1 phase and apoptosis. On the opposite, circ_0007031 overexpression promoted cell proliferation and induced cell arrest at S phase. Additionally, miR-485-3p inhibitors attenuated circ_0007031 silencing-mediated CRC cell malignancy. MiR-485-3p was unveiled to regulate CRC cell processes via targeting MELK. Circ_0007031 controlled MELK expression via interacting with miR-485-3p. Furthermore, circ_0007031 contributed to tumor formation in vivo. Circ_0007031 knockdown repressed CRC malignant progression by reducing MELK expression through associating with miR-485-3p, suggesting that circ_0007031 was a potential target for the therapy of CRC. |
| doi_str_mv | 10.1007/s10528-021-10111-5 |
| format | Article |
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Circular RNA (circRNA) is recently found to participate in the regulation of CRC progression. However, the role of circ_0007031 in CRC malignant progression remains elusive. 50 CRC patients were implicated in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the RNA expression of circ_0007031, microRNA-485-3p (miR-485-3p) and maternal embryonic leucine zipper kinase (MELK). Western blot analysis was conducted to determine protein expression. Cell viability and proliferation were demonstrated by cell counting kit-8 and 5-Ethynyl-29-deoxyuridine (EdU) assays, respectively. Cell cycle and apoptosis were investigated by flow cytometry analysis. The interaction among circ_0007031, miR-485-3p and MELK was predicted by online databases, and identified by dual-luciferase reporter assay. Mouse model assay was conducted to reveal the effect of circ_0007031 on tumor formation in vivo. Circ_0007031 and MELK expression were obviously increased, while miR-485-3p expression was decreased in CRC tissues and cells compared with normal colorectal tissues or cells. Circ_0007031 knockdown repressed proliferation, whereas induced cell arrest at G0/G1 phase and apoptosis. On the opposite, circ_0007031 overexpression promoted cell proliferation and induced cell arrest at S phase. Additionally, miR-485-3p inhibitors attenuated circ_0007031 silencing-mediated CRC cell malignancy. MiR-485-3p was unveiled to regulate CRC cell processes via targeting MELK. Circ_0007031 controlled MELK expression via interacting with miR-485-3p. Furthermore, circ_0007031 contributed to tumor formation in vivo. Circ_0007031 knockdown repressed CRC malignant progression by reducing MELK expression through associating with miR-485-3p, suggesting that circ_0007031 was a potential target for the therapy of CRC.</description><identifier>ISSN: 0006-2928</identifier><identifier>EISSN: 1573-4927</identifier><identifier>DOI: 10.1007/s10528-021-10111-5</identifier><identifier>PMID: 34322757</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Assaying ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Cell cycle ; Cell growth ; Cell proliferation ; Cell Proliferation - genetics ; Cell viability ; Circular RNA ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - metabolism ; Embryos ; Flow cytometry ; G1 phase ; Gene expression ; Human Genetics ; Humans ; Kinases ; Leucine ; Leucine zipper proteins ; Malignancy ; Medical Microbiology ; Mice ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Original Article ; Polymerase chain reaction ; Protein Serine-Threonine Kinases ; Ribonucleic acid ; RNA ; RNA, Circular - genetics ; S phase ; Tumors ; Zoology</subject><ispartof>Biochemical genetics, 2022-04, Vol.60 (2), p.576-597</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-ae2c8d31b20ce1e9c7882684c2ad0073dd781a501088b3defd258f830460c923</citedby><cites>FETCH-LOGICAL-c375t-ae2c8d31b20ce1e9c7882684c2ad0073dd781a501088b3defd258f830460c923</cites><orcidid>0000-0002-1690-8481</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/s10528-021-10111-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10528-021-10111-5$$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/34322757$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Shengtian</creatorcontrib><creatorcontrib>Lu, Wenjing</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><creatorcontrib>Li, Liping</creatorcontrib><creatorcontrib>Liu, Liang</creatorcontrib><creatorcontrib>Li, Xiaoju</creatorcontrib><creatorcontrib>Ye, Dan</creatorcontrib><creatorcontrib>Yu, Zhigao</creatorcontrib><title>Circ_0007031 Silencing Inhibits Cell Proliferation and Induces Cell Apoptosis via Downregulating MELK at a miR-485-3p-Dependent Way in Colorectal Cancer</title><title>Biochemical genetics</title><addtitle>Biochem Genet</addtitle><addtitle>Biochem Genet</addtitle><description>Colorectal cancer (CRC) is a malignant cancer with an increasing incidence. Circular RNA (circRNA) is recently found to participate in the regulation of CRC progression. However, the role of circ_0007031 in CRC malignant progression remains elusive. 50 CRC patients were implicated in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the RNA expression of circ_0007031, microRNA-485-3p (miR-485-3p) and maternal embryonic leucine zipper kinase (MELK). Western blot analysis was conducted to determine protein expression. Cell viability and proliferation were demonstrated by cell counting kit-8 and 5-Ethynyl-29-deoxyuridine (EdU) assays, respectively. Cell cycle and apoptosis were investigated by flow cytometry analysis. The interaction among circ_0007031, miR-485-3p and MELK was predicted by online databases, and identified by dual-luciferase reporter assay. Mouse model assay was conducted to reveal the effect of circ_0007031 on tumor formation in vivo. Circ_0007031 and MELK expression were obviously increased, while miR-485-3p expression was decreased in CRC tissues and cells compared with normal colorectal tissues or cells. Circ_0007031 knockdown repressed proliferation, whereas induced cell arrest at G0/G1 phase and apoptosis. On the opposite, circ_0007031 overexpression promoted cell proliferation and induced cell arrest at S phase. Additionally, miR-485-3p inhibitors attenuated circ_0007031 silencing-mediated CRC cell malignancy. MiR-485-3p was unveiled to regulate CRC cell processes via targeting MELK. Circ_0007031 controlled MELK expression via interacting with miR-485-3p. Furthermore, circ_0007031 contributed to tumor formation in vivo. Circ_0007031 knockdown repressed CRC malignant progression by reducing MELK expression through associating with miR-485-3p, suggesting that circ_0007031 was a potential target for the therapy of CRC.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Assaying</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell viability</subject><subject>Circular RNA</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Embryos</subject><subject>Flow cytometry</subject><subject>G1 phase</subject><subject>Gene expression</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Leucine</subject><subject>Leucine zipper proteins</subject><subject>Malignancy</subject><subject>Medical Microbiology</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Original Article</subject><subject>Polymerase chain reaction</subject><subject>Protein Serine-Threonine Kinases</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Circular - genetics</subject><subject>S phase</subject><subject>Tumors</subject><subject>Zoology</subject><issn>0006-2928</issn><issn>1573-4927</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1DAURi1ERaeFF2CBLLFhY_Bv4iyrtNCKqUBQiaXlsW8GVxk72Amob8Lj1jADSCy6sqzv3M--Ogg9Z_Q1o7R9UxhVXBPKGWGUMUbUI7RiqhVEdrx9jFaU0obwjutjdFLKbb12VMon6FhIwXmr2hX62YfsTE1aKhj-HEaILsQtvopfwybMBfcwjvhjTmMYINs5pIht9DX3i4NDfDalaU4lFPw9WHyefsQM22WsdG26vli_x3bGFu_CJyK1ImIi5zBB9BBn_MXe4RBxn8aUwc12xL2NDvJTdDTYscCzw3mKbt5e3PSXZP3h3VV_tiZOtGomFrjTXrANpw4YdK7VmjdaOm59XUp432pmFWVU643wMHiu9KAFlQ11HRen6NW-dsrp2wJlNrtQXF3KRkhLMVypRmjJpKzoy__Q27TkWD9neCNp03QVrBTfUy6nUjIMZsphZ_OdYdT80mb22kzVZn5rM6oOvThUL5sd-L8jfzxVQOyBUqO4hfzv7Qdq7wE92KBq</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Su, Shengtian</creator><creator>Lu, Wenjing</creator><creator>Liu, Jun</creator><creator>Li, Liping</creator><creator>Liu, Liang</creator><creator>Li, Xiaoju</creator><creator>Ye, Dan</creator><creator>Yu, Zhigao</creator><general>Springer US</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>7SS</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1690-8481</orcidid></search><sort><creationdate>20220401</creationdate><title>Circ_0007031 Silencing Inhibits Cell Proliferation and Induces Cell Apoptosis via Downregulating MELK at a miR-485-3p-Dependent Way in Colorectal Cancer</title><author>Su, Shengtian ; Lu, Wenjing ; Liu, Jun ; Li, Liping ; Liu, Liang ; Li, Xiaoju ; Ye, Dan ; Yu, Zhigao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-ae2c8d31b20ce1e9c7882684c2ad0073dd781a501088b3defd258f830460c923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><jtitle>Biochemical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Shengtian</au><au>Lu, Wenjing</au><au>Liu, Jun</au><au>Li, Liping</au><au>Liu, Liang</au><au>Li, Xiaoju</au><au>Ye, Dan</au><au>Yu, Zhigao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circ_0007031 Silencing Inhibits Cell Proliferation and Induces Cell Apoptosis via Downregulating MELK at a miR-485-3p-Dependent Way in Colorectal Cancer</atitle><jtitle>Biochemical genetics</jtitle><stitle>Biochem Genet</stitle><addtitle>Biochem Genet</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>60</volume><issue>2</issue><spage>576</spage><epage>597</epage><pages>576-597</pages><issn>0006-2928</issn><eissn>1573-4927</eissn><abstract>Colorectal cancer (CRC) is a malignant cancer with an increasing incidence. Circular RNA (circRNA) is recently found to participate in the regulation of CRC progression. However, the role of circ_0007031 in CRC malignant progression remains elusive. 50 CRC patients were implicated in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the RNA expression of circ_0007031, microRNA-485-3p (miR-485-3p) and maternal embryonic leucine zipper kinase (MELK). Western blot analysis was conducted to determine protein expression. Cell viability and proliferation were demonstrated by cell counting kit-8 and 5-Ethynyl-29-deoxyuridine (EdU) assays, respectively. Cell cycle and apoptosis were investigated by flow cytometry analysis. The interaction among circ_0007031, miR-485-3p and MELK was predicted by online databases, and identified by dual-luciferase reporter assay. Mouse model assay was conducted to reveal the effect of circ_0007031 on tumor formation in vivo. Circ_0007031 and MELK expression were obviously increased, while miR-485-3p expression was decreased in CRC tissues and cells compared with normal colorectal tissues or cells. Circ_0007031 knockdown repressed proliferation, whereas induced cell arrest at G0/G1 phase and apoptosis. On the opposite, circ_0007031 overexpression promoted cell proliferation and induced cell arrest at S phase. Additionally, miR-485-3p inhibitors attenuated circ_0007031 silencing-mediated CRC cell malignancy. MiR-485-3p was unveiled to regulate CRC cell processes via targeting MELK. Circ_0007031 controlled MELK expression via interacting with miR-485-3p. Furthermore, circ_0007031 contributed to tumor formation in vivo. Circ_0007031 knockdown repressed CRC malignant progression by reducing MELK expression through associating with miR-485-3p, suggesting that circ_0007031 was a potential target for the therapy of CRC.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34322757</pmid><doi>10.1007/s10528-021-10111-5</doi><tpages>22</tpages><orcidid>https://orcid.org/0000-0002-1690-8481</orcidid></addata></record> |
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| ispartof | Biochemical genetics, 2022-04, Vol.60 (2), p.576-597 |
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| subjects | Animals Apoptosis Apoptosis - genetics Assaying Biochemistry Biomedical and Life Sciences Biomedicine Cancer Cell cycle Cell growth Cell proliferation Cell Proliferation - genetics Cell viability Circular RNA Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - metabolism Embryos Flow cytometry G1 phase Gene expression Human Genetics Humans Kinases Leucine Leucine zipper proteins Malignancy Medical Microbiology Mice MicroRNAs - genetics MicroRNAs - metabolism miRNA Original Article Polymerase chain reaction Protein Serine-Threonine Kinases Ribonucleic acid RNA RNA, Circular - genetics S phase Tumors Zoology |
| title | Circ_0007031 Silencing Inhibits Cell Proliferation and Induces Cell Apoptosis via Downregulating MELK at a miR-485-3p-Dependent Way in Colorectal Cancer |
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