Downregulation of Foxc2 enhances apoptosis induced by 5-fluorouracil through activation of MAPK and AKT pathways in colorectal cancer
Identifieur interne : 000690 ( Pmc/Corpus ); précédent : 000689; suivant : 000691Downregulation of Foxc2 enhances apoptosis induced by 5-fluorouracil through activation of MAPK and AKT pathways in colorectal cancer
Auteurs : Chao Yang ; Xiaoxian Cui ; Xiaoqin Dai ; Wenting LiaoSource :
- Oncology Letters [ 1792-1074 ] ; 2016.
Abstract
The chemotherapy drug 5-fluorouracil (5-FU) is fundamental for the treatment of colorectal cancer (CRC); however, drug resistance to 5-FU may occasionally occur. Abnormal expression of Forkhead box C2 gene (Foxc2) has been identified in several human cancers, but the role of Foxc2 in the progression of CRC remains unclear. The present study established a stable Foxc2-short hairpin (sh)RNA cell line, which was confirmed by western blot analysis and quantitative polymerase chain reaction. The Foxc2-shRNA cells were treated with 5-FU and the cell viability was determined by an MTT assay. Western blot analysis was performed to investigate the signaling pathway involved in 5-FU treatment. The present study identified that 5-FU increased the percentage of apoptotic CRC cells among the Foxc2/RNA interference-transfected cells compared with cells transfected with an empty vector. Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Furthermore, the mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathways were essential for the sensitization effect of Foxc2 to 5-FU treatment. Overall, these findings reveal the mechanisms behind Foxc2 depletion and 5-FU treatment of CRC and suggest that Foxc2 enhances resistance to apoptosis, induced by 5-FU, through the activation of MAPK and P13K/AKT pathways, and may serve as a valuable clinical prognostic marker for CRC.
Url:
DOI: 10.3892/ol.2016.4097
PubMed: 26893778
PubMed Central: 4734250
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PMC:4734250Le document en format XML
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<author><name sortKey="Yang, Chao" sort="Yang, Chao" uniqKey="Yang C" first="Chao" last="Yang">Chao Yang</name>
<affiliation><nlm:aff id="af1-ol-0-0-4097">Department of Pathology, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China</nlm:aff>
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<author><name sortKey="Liao, Wenting" sort="Liao, Wenting" uniqKey="Liao W" first="Wenting" last="Liao">Wenting Liao</name>
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<series><title level="j">Oncology Letters</title>
<idno type="ISSN">1792-1074</idno>
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<front><div type="abstract" xml:lang="en"><p>The chemotherapy drug 5-fluorouracil (5-FU) is fundamental for the treatment of colorectal cancer (CRC); however, drug resistance to 5-FU may occasionally occur. Abnormal expression of Forkhead box C2 gene (Foxc2) has been identified in several human cancers, but the role of Foxc2 in the progression of CRC remains unclear. The present study established a stable Foxc2-short hairpin (sh)RNA cell line, which was confirmed by western blot analysis and quantitative polymerase chain reaction. The Foxc2-shRNA cells were treated with 5-FU and the cell viability was determined by an MTT assay. Western blot analysis was performed to investigate the signaling pathway involved in 5-FU treatment. The present study identified that 5-FU increased the percentage of apoptotic CRC cells among the Foxc2/RNA interference-transfected cells compared with cells transfected with an empty vector. Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Furthermore, the mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathways were essential for the sensitization effect of Foxc2 to 5-FU treatment. Overall, these findings reveal the mechanisms behind Foxc2 depletion and 5-FU treatment of CRC and suggest that Foxc2 enhances resistance to apoptosis, induced by 5-FU, through the activation of MAPK and P13K/AKT pathways, and may serve as a valuable clinical prognostic marker for CRC.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Oncol Lett</journal-id>
<journal-id journal-id-type="iso-abbrev">Oncol Lett</journal-id>
<journal-id journal-id-type="publisher-id">OL</journal-id>
<journal-title-group><journal-title>Oncology Letters</journal-title>
</journal-title-group>
<issn pub-type="ppub">1792-1074</issn>
<issn pub-type="epub">1792-1082</issn>
<publisher><publisher-name>D.A. Spandidos</publisher-name>
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<article-meta><article-id pub-id-type="pmid">26893778</article-id>
<article-id pub-id-type="pmc">4734250</article-id>
<article-id pub-id-type="doi">10.3892/ol.2016.4097</article-id>
<article-id pub-id-type="publisher-id">OL-0-0-4097</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>Downregulation of Foxc2 enhances apoptosis induced by 5-fluorouracil through activation of MAPK and AKT pathways in colorectal cancer</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>YANG</surname>
<given-names>CHAO</given-names>
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<xref ref-type="aff" rid="af1-ol-0-0-4097">1</xref>
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<contrib contrib-type="author"><name><surname>CUI</surname>
<given-names>XIAOXIAN</given-names>
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<contrib contrib-type="author"><name><surname>DAI</surname>
<given-names>XIAOQIN</given-names>
</name>
<xref ref-type="aff" rid="af1-ol-0-0-4097">1</xref>
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<contrib contrib-type="author"><name><surname>LIAO</surname>
<given-names>WENTING</given-names>
</name>
<xref ref-type="aff" rid="af1-ol-0-0-4097">1</xref>
<xref ref-type="aff" rid="af2-ol-0-0-4097">2</xref>
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<aff id="af1-ol-0-0-4097"><label>1</label>
Department of Pathology, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China</aff>
<aff id="af2-ol-0-0-4097"><label>2</label>
Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China</aff>
<author-notes><corresp id="c1-ol-0-0-4097"><italic>Correspondence to</italic>
: Dr Wenting Liao, Department of Pathology, Nanfang Hospital, Southern Medical University, 1838 North Avenue, Guangzhou, Guangdong 510515, P.R. China, E-mail: <email>liaowt2002@gmail.com</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>2</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>08</day>
<month>1</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>08</day>
<month>1</month>
<year>2016</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>11</volume>
<issue>2</issue>
<fpage>1549</fpage>
<lpage>1554</lpage>
<history><date date-type="received"><day>06</day>
<month>2</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>18</day>
<month>12</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016, Spandidos Publications</copyright-statement>
<copyright-year>2016</copyright-year>
</permissions>
<abstract><p>The chemotherapy drug 5-fluorouracil (5-FU) is fundamental for the treatment of colorectal cancer (CRC); however, drug resistance to 5-FU may occasionally occur. Abnormal expression of Forkhead box C2 gene (Foxc2) has been identified in several human cancers, but the role of Foxc2 in the progression of CRC remains unclear. The present study established a stable Foxc2-short hairpin (sh)RNA cell line, which was confirmed by western blot analysis and quantitative polymerase chain reaction. The Foxc2-shRNA cells were treated with 5-FU and the cell viability was determined by an MTT assay. Western blot analysis was performed to investigate the signaling pathway involved in 5-FU treatment. The present study identified that 5-FU increased the percentage of apoptotic CRC cells among the Foxc2/RNA interference-transfected cells compared with cells transfected with an empty vector. Therefore, the downregulation of Foxc2, induced by 5-FU, may enhance apoptosis by the downregulation of apoptotic factors, including B cell lymphoma-2 and pro-caspase-3, in Foxc2-shRNA CRC cells. Furthermore, the mitogen-activated protein kinase (MAPK) and phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathways were essential for the sensitization effect of Foxc2 to 5-FU treatment. Overall, these findings reveal the mechanisms behind Foxc2 depletion and 5-FU treatment of CRC and suggest that Foxc2 enhances resistance to apoptosis, induced by 5-FU, through the activation of MAPK and P13K/AKT pathways, and may serve as a valuable clinical prognostic marker for CRC.</p>
</abstract>
<kwd-group><kwd>colorectal cancer</kwd>
<kwd>Foxc2</kwd>
<kwd>apoptosis</kwd>
<kwd>MAPK</kwd>
<kwd>AKT</kwd>
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