Periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway

In the present study, we aimed to explore the effects of periostin, a cell adhesion protein, on chemoresistance in colon cancer cells. Reverse‐transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT‐29 colon cancer cells treated...

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Veröffentlicht in:Biotechnology and applied biochemistry 2015-05, Vol.62 (3), p.401-406
Hauptverfasser: Xiao, Zhi-ming, Wang, Xiao-yan, Wang, Ai-min
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Wang, Xiao-yan
Wang, Ai-min
description In the present study, we aimed to explore the effects of periostin, a cell adhesion protein, on chemoresistance in colon cancer cells. Reverse‐transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT‐29 colon cancer cells treated with oxaliplatin or fluorouracil (5‐FU). Small interfering RNA was used to downregulate endogenous periostin. Annexin‐V/propidium iodide staining was performed to analyze the effects of periostin on drug‐induced apoptosis. The results showed that treatment with oxaliplatin or 5‐FU elevated both the mRNA and protein levels of periostin in SW480 and HT‐29 cells. Silencing of periostin significantly (P 
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Reverse‐transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT‐29 colon cancer cells treated with oxaliplatin or fluorouracil (5‐FU). Small interfering RNA was used to downregulate endogenous periostin. Annexin‐V/propidium iodide staining was performed to analyze the effects of periostin on drug‐induced apoptosis. The results showed that treatment with oxaliplatin or 5‐FU elevated both the mRNA and protein levels of periostin in SW480 and HT‐29 cells. Silencing of periostin significantly (P &lt; 0.01) augmented drug‐induced apoptosis in colon cancer cells, coupled with enhanced cleavage of caspase‐3 and poly(ADP‐ribose) polymerase. Mechanistic studies revealed that periostin silencing significantly (P &lt; 0.01) suppressed the expression of survivin, an antiapoptotic protein in colon cancer cells. Enforced expression of survivin repressed drug‐induced apoptosis in periostin‐depleted SW480 and HT‐29 cells. Additionally, periostin overexpression increased the expression of survivin and the phosphorylation of Akt, which was reversed by pretreatment with the phosphatidylinositol 3‐kinase (PI3K)‐specific inhibitor LY294002. Taken together, our data demonstrate that periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway.</description><identifier>ISSN: 0885-4513</identifier><identifier>EISSN: 1470-8744</identifier><identifier>DOI: 10.1002/bab.1193</identifier><identifier>PMID: 24372557</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Activation ; Apoptosis ; Cancer ; Cell Adhesion Molecules - antagonists &amp; inhibitors ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; Cell Adhesion Molecules - pharmacology ; Cell Line, Tumor ; chemotherapy ; Colon ; Colonic Neoplasms - metabolism ; drug resistance ; Drug Resistance, Neoplasm - drug effects ; Fluorouracil - pharmacology ; Humans ; Inhibitors ; Organoplatinum Compounds - pharmacology ; Pathways ; periostin ; Phosphatidylinositol 3-Kinases - metabolism ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Ribonucleic acids ; Signal Transduction - drug effects ; signaling pathway</subject><ispartof>Biotechnology and applied biochemistry, 2015-05, Vol.62 (3), p.401-406</ispartof><rights>2013 International Union of Biochemistry and Molecular Biology, Inc.</rights><rights>Copyright © 2015 International Union of Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fbab.1193$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fbab.1193$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24372557$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Zhi-ming</creatorcontrib><creatorcontrib>Wang, Xiao-yan</creatorcontrib><creatorcontrib>Wang, Ai-min</creatorcontrib><title>Periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway</title><title>Biotechnology and applied biochemistry</title><addtitle>Biotechnology and Applied Biochemistry</addtitle><description>In the present study, we aimed to explore the effects of periostin, a cell adhesion protein, on chemoresistance in colon cancer cells. Reverse‐transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT‐29 colon cancer cells treated with oxaliplatin or fluorouracil (5‐FU). Small interfering RNA was used to downregulate endogenous periostin. Annexin‐V/propidium iodide staining was performed to analyze the effects of periostin on drug‐induced apoptosis. The results showed that treatment with oxaliplatin or 5‐FU elevated both the mRNA and protein levels of periostin in SW480 and HT‐29 cells. Silencing of periostin significantly (P &lt; 0.01) augmented drug‐induced apoptosis in colon cancer cells, coupled with enhanced cleavage of caspase‐3 and poly(ADP‐ribose) polymerase. Mechanistic studies revealed that periostin silencing significantly (P &lt; 0.01) suppressed the expression of survivin, an antiapoptotic protein in colon cancer cells. Enforced expression of survivin repressed drug‐induced apoptosis in periostin‐depleted SW480 and HT‐29 cells. Additionally, periostin overexpression increased the expression of survivin and the phosphorylation of Akt, which was reversed by pretreatment with the phosphatidylinositol 3‐kinase (PI3K)‐specific inhibitor LY294002. Taken together, our data demonstrate that periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway.</description><subject>Activation</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell Adhesion Molecules - antagonists &amp; inhibitors</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Adhesion Molecules - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>chemotherapy</subject><subject>Colon</subject><subject>Colonic Neoplasms - metabolism</subject><subject>drug resistance</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Fluorouracil - pharmacology</subject><subject>Humans</subject><subject>Inhibitors</subject><subject>Organoplatinum Compounds - pharmacology</subject><subject>Pathways</subject><subject>periostin</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Ribonucleic acids</subject><subject>Signal Transduction - drug effects</subject><subject>signaling pathway</subject><issn>0885-4513</issn><issn>1470-8744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EoktB4hegSFy4pDuOv4_bFbQVS6kECImLZScO62423trJtvvvcdRSJC5w8cjvPB6N9SD0GsMJBqjm1tgTjBV5gmaYCiiloPQpmoGUrKQMkyP0IqVrAJBCVs_RUUWJqBgTM7S5ctGHNPi-8H0z1i4V9dptQ3TJp8H0tct5UYcu5HO6xqJ2XZeKYR3D-HNdmHrwezP43A9tTl1xdUE-zhebYZ7GuPf7_HxnhvWtObxEz1rTJffqoR6jbx_ef12el6vPZxfLxar0066loowQ7JRogHGCK2ppI7lsbJPjVkjgvLUMbNMaSxQIJwmzjQWgSmJbS3KM3t3P3cVwM7o06K1P09amd2FMGgtQghIuqv9BMZUYE_JvlCuoMAfCM_r2L_Q6jLHPf86UVFxipUSm3jxQo926Ru-i35p40L_lZKC8B2595w6PfQx6kq6zdD1J16eL06n-4bM5d_fIm7jRXBDB9PfLM_1jeVl9Wn7hekV-ARHyq3E</recordid><startdate>201505</startdate><enddate>201505</enddate><creator>Xiao, Zhi-ming</creator><creator>Wang, Xiao-yan</creator><creator>Wang, Ai-min</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TB</scope><scope>7TK</scope><scope>7U5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>L7M</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201505</creationdate><title>Periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway</title><author>Xiao, Zhi-ming ; 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Reverse‐transcription polymerase chain reaction and Western blot analyses were employed to detect periostin expression in SW480 and HT‐29 colon cancer cells treated with oxaliplatin or fluorouracil (5‐FU). Small interfering RNA was used to downregulate endogenous periostin. Annexin‐V/propidium iodide staining was performed to analyze the effects of periostin on drug‐induced apoptosis. The results showed that treatment with oxaliplatin or 5‐FU elevated both the mRNA and protein levels of periostin in SW480 and HT‐29 cells. Silencing of periostin significantly (P &lt; 0.01) augmented drug‐induced apoptosis in colon cancer cells, coupled with enhanced cleavage of caspase‐3 and poly(ADP‐ribose) polymerase. Mechanistic studies revealed that periostin silencing significantly (P &lt; 0.01) suppressed the expression of survivin, an antiapoptotic protein in colon cancer cells. Enforced expression of survivin repressed drug‐induced apoptosis in periostin‐depleted SW480 and HT‐29 cells. Additionally, periostin overexpression increased the expression of survivin and the phosphorylation of Akt, which was reversed by pretreatment with the phosphatidylinositol 3‐kinase (PI3K)‐specific inhibitor LY294002. Taken together, our data demonstrate that periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>24372557</pmid><doi>10.1002/bab.1193</doi><tpages>6</tpages></addata></record>
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subjects Activation
Apoptosis
Cancer
Cell Adhesion Molecules - antagonists & inhibitors
Cell Adhesion Molecules - genetics
Cell Adhesion Molecules - metabolism
Cell Adhesion Molecules - pharmacology
Cell Line, Tumor
chemotherapy
Colon
Colonic Neoplasms - metabolism
drug resistance
Drug Resistance, Neoplasm - drug effects
Fluorouracil - pharmacology
Humans
Inhibitors
Organoplatinum Compounds - pharmacology
Pathways
periostin
Phosphatidylinositol 3-Kinases - metabolism
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Ribonucleic acids
Signal Transduction - drug effects
signaling pathway
title Periostin induces chemoresistance in colon cancer cells through activation of the PI3K/Akt/survivin pathway
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