KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p
Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in N...
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| Veröffentlicht in: | Cell biochemistry and function 2019-08, Vol.37 (6), p.424-431 |
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| creator | Gan, Huizhu Lin, Lin Hu, Nanjun Yang, Yang Gao, Yu Pei, Yu Chen, Kang Sun, Butong |
| description | Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P |
| doi_str_mv | 10.1002/cbf.3420 |
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Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P < .0001). We also proved that the high expression level of KIF2C predicted worse prognosis of the patients. After knockdown of KIF2C, the proliferation and metastasis of NSCLC cells were inhibited. Luciferase reporter assay suggested that KIF2C was a target gene of miR‐325‐3p, which was reported to be a tumour suppressor in NSCLC. In conclusion, this study proved an oncogenic role of KIF2C in NSCLC and partly clarified the mechanism of its high expression. Our findings provided a useful insight into the mechanism of NSCLC progression and offered clues to novel therapy strategies.</description><identifier>ISSN: 0263-6484</identifier><identifier>EISSN: 1099-0844</identifier><identifier>DOI: 10.1002/cbf.3420</identifier><identifier>PMID: 31328811</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Carcinogenesis - genetics ; Carcinogenesis - metabolism ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell proliferation ; Chromosome 3 ; Chromosomes ; Depolymerization ; Humans ; KIF2C ; Kinesin ; Kinesin - genetics ; Kinesin - metabolism ; Lung cancer ; Lymph nodes ; Metastases ; Metastasis ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR‐325‐3p ; Non-small cell lung carcinoma ; nonsmall cell lung cancer ; pathology ; Tumors</subject><ispartof>Cell biochemistry and function, 2019-08, Vol.37 (6), p.424-431</ispartof><rights>2019 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3490-1562d0ee294b30cb941352bec500e856c9287f1a40bf2312f1c5c83cd9a92f613</citedby><cites>FETCH-LOGICAL-c3490-1562d0ee294b30cb941352bec500e856c9287f1a40bf2312f1c5c83cd9a92f613</cites><orcidid>0000-0001-8333-357X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcbf.3420$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcbf.3420$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31328811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gan, Huizhu</creatorcontrib><creatorcontrib>Lin, Lin</creatorcontrib><creatorcontrib>Hu, Nanjun</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Gao, Yu</creatorcontrib><creatorcontrib>Pei, Yu</creatorcontrib><creatorcontrib>Chen, Kang</creatorcontrib><creatorcontrib>Sun, Butong</creatorcontrib><title>KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p</title><title>Cell biochemistry and function</title><addtitle>Cell Biochem Funct</addtitle><description>Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P < .0001). We also proved that the high expression level of KIF2C predicted worse prognosis of the patients. After knockdown of KIF2C, the proliferation and metastasis of NSCLC cells were inhibited. Luciferase reporter assay suggested that KIF2C was a target gene of miR‐325‐3p, which was reported to be a tumour suppressor in NSCLC. In conclusion, this study proved an oncogenic role of KIF2C in NSCLC and partly clarified the mechanism of its high expression. Our findings provided a useful insight into the mechanism of NSCLC progression and offered clues to novel therapy strategies.</description><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Chromosome 3</subject><subject>Chromosomes</subject><subject>Depolymerization</subject><subject>Humans</subject><subject>KIF2C</subject><subject>Kinesin</subject><subject>Kinesin - genetics</subject><subject>Kinesin - metabolism</subject><subject>Lung cancer</subject><subject>Lymph nodes</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR‐325‐3p</subject><subject>Non-small cell lung carcinoma</subject><subject>nonsmall cell lung cancer</subject><subject>pathology</subject><subject>Tumors</subject><issn>0263-6484</issn><issn>1099-0844</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtKxDAUhoMoOl7AJ5CAGzcdTy6NzVIHR0VBEF2XND0dIm06JlN1dj6Cz-iT2HoFwc05m4-Pn4-QXQZjBsAPbVGNheSwQkYMtE4gk3KVjIArkSiZyQ2yGeM9AGglYJ1sCCZ4ljE2Iu7yYsonFJ8xLCI1nrbetjP0ztLQ1kidp771sTF1TS32p-78jFrjLYYeL6mL1OPMLNwj1ksacNbVZoElLZa0cTdvL6-Cp8Odb5O1ytQRd77-Frmbnt5OzpOr67OLyfFVYoXUkLBU8RIQuZaFAFtoyUTKC7QpAGapsppnRxUzEoqKC8YrZlObCVtqo3mlmNgiB5_eeWgfOoyLvHFxmG48tl3MOVdMH0n9ge7_Qe_bLvh-3UBpDkoB_AptaGMMWOXz4BoTljmDfMif9_nzIX-P7n0Ju6LB8gf87t0DySfw5Gpc_ivKJyfTD-E7XFCNFA</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>Gan, Huizhu</creator><creator>Lin, Lin</creator><creator>Hu, Nanjun</creator><creator>Yang, Yang</creator><creator>Gao, Yu</creator><creator>Pei, Yu</creator><creator>Chen, Kang</creator><creator>Sun, Butong</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8333-357X</orcidid></search><sort><creationdate>201908</creationdate><title>KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p</title><author>Gan, Huizhu ; Lin, Lin ; Hu, Nanjun ; Yang, Yang ; Gao, Yu ; Pei, Yu ; Chen, Kang ; Sun, Butong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3490-1562d0ee294b30cb941352bec500e856c9287f1a40bf2312f1c5c83cd9a92f613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Chromosome 3</topic><topic>Chromosomes</topic><topic>Depolymerization</topic><topic>Humans</topic><topic>KIF2C</topic><topic>Kinesin</topic><topic>Kinesin - genetics</topic><topic>Kinesin - metabolism</topic><topic>Lung cancer</topic><topic>Lymph nodes</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR‐325‐3p</topic><topic>Non-small cell lung carcinoma</topic><topic>nonsmall cell lung cancer</topic><topic>pathology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gan, Huizhu</creatorcontrib><creatorcontrib>Lin, Lin</creatorcontrib><creatorcontrib>Hu, Nanjun</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Gao, Yu</creatorcontrib><creatorcontrib>Pei, Yu</creatorcontrib><creatorcontrib>Chen, Kang</creatorcontrib><creatorcontrib>Sun, Butong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and function</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gan, Huizhu</au><au>Lin, Lin</au><au>Hu, Nanjun</au><au>Yang, Yang</au><au>Gao, Yu</au><au>Pei, Yu</au><au>Chen, Kang</au><au>Sun, Butong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p</atitle><jtitle>Cell biochemistry and function</jtitle><addtitle>Cell Biochem Funct</addtitle><date>2019-08</date><risdate>2019</risdate><volume>37</volume><issue>6</issue><spage>424</spage><epage>431</epage><pages>424-431</pages><issn>0263-6484</issn><eissn>1099-0844</eissn><abstract>Nonsmall cell lung cancer (NSCLC) is one of the leading causes of cancer‐related death worldwide. Kinesin family member 2C (KIF2C), a modulator in microtubule depolymerization, bipolar spindle formation, and chromosome segregation, has been reported to take roles in cancer biology, but its role in NSCLC remains unclear. This study was intended to investigate the expression and function of KIF2C in NSCLC. Our results demonstrated that KIF2C was up‐regulated in NSCLC tissues and cell lines. The high expression of KIF2C in NSCLC tissues was significantly correlated with higher T stage (0.0078), worse differentiation status (0.0049), and lymph node metastasis (P < .0001). We also proved that the high expression level of KIF2C predicted worse prognosis of the patients. After knockdown of KIF2C, the proliferation and metastasis of NSCLC cells were inhibited. Luciferase reporter assay suggested that KIF2C was a target gene of miR‐325‐3p, which was reported to be a tumour suppressor in NSCLC. 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| ispartof | Cell biochemistry and function, 2019-08, Vol.37 (6), p.424-431 |
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| subjects | Carcinogenesis - genetics Carcinogenesis - metabolism Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell proliferation Chromosome 3 Chromosomes Depolymerization Humans KIF2C Kinesin Kinesin - genetics Kinesin - metabolism Lung cancer Lymph nodes Metastases Metastasis MicroRNAs - genetics MicroRNAs - metabolism miR‐325‐3p Non-small cell lung carcinoma nonsmall cell lung cancer pathology Tumors |
| title | KIF2C exerts an oncogenic role in nonsmall cell lung cancer and is negatively regulated by miR‐325‐3p |
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