Peroxiredoxin 2 is upregulated in colorectal cancer and contributes to colorectal cancer cells’ survival by protecting cells from oxidative stress
Peroxiredoxin 2 (Prdx2) is a member of the peroxiredoxin family, which is responsible for neutralizing reactive oxygen species. Prdx2 has been found to be elevated in several human cancer cells and tissues, including colorectal cancer (CRC), and it influences diverse cellular processes involving cel...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2014-02, Vol.387 (1-2), p.261-270 |
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| creator | Lu, Weidong Fu, Zhongxue Wang, Hao Feng, Jihong Wei, Jinlai Guo, Jinbao |
| description | Peroxiredoxin 2 (Prdx2) is a member of the peroxiredoxin family, which is responsible for neutralizing reactive oxygen species. Prdx2 has been found to be elevated in several human cancer cells and tissues, including colorectal cancer (CRC), and it influences diverse cellular processes involving cells’ survival, proliferation, and apoptosis, which suggests a possible role for Prdx2 in the maintenance of cancer cell. However, the mechanism by which Prdx2 modulates CRC cells’ survival is unknown. The current study aimed to determine the effect of elevated Prdx2 on CRC cells and to further understand the underlying mechanisms. The results of this study showed that Prdx2 was upregulated in CRC tissues compared with the matched noncancer colorectal mucosa tissues and that Prdx2 expression was positively associated with tumor metastasis and the TNM stage. In the LoVo CRC cell line, Prdx2 was upregulated at both the RNA and protein levels compared with the normal FHC colorectal mucosa cell line. In addition, the LoVo CRC cell line was significantly more resistant to hydrogen peroxide (H
2
O
2
)-induced apoptosis because of a failure to activate pro-apoptotic pathways in contrast to Prdx2 knockdown cells. Suppression of Prdx2 using a lentiviral vector-mediated Prdx2-specific shRNA in the LoVo cell line restored H
2
O
2
sensitivity. Our results suggested that Prdx2 has an essential role in regulating oxidation-induced apoptosis in CRC cells. Prdx2 may have potential as a therapeutic target in CRC. |
| doi_str_mv | 10.1007/s11010-013-1891-4 |
| format | Article |
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2
O
2
)-induced apoptosis because of a failure to activate pro-apoptotic pathways in contrast to Prdx2 knockdown cells. Suppression of Prdx2 using a lentiviral vector-mediated Prdx2-specific shRNA in the LoVo cell line restored H
2
O
2
sensitivity. Our results suggested that Prdx2 has an essential role in regulating oxidation-induced apoptosis in CRC cells. Prdx2 may have potential as a therapeutic target in CRC.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-013-1891-4</identifier><identifier>PMID: 24234423</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adenocarcinoma - enzymology ; Adenocarcinoma - pathology ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cancer cells ; Cardiology ; Cell Line, Tumor ; Cell Survival ; Cellular biology ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - enzymology ; Colorectal Neoplasms - pathology ; Disease Progression ; Enzymes ; Female ; Gene Expression ; Health aspects ; Humans ; Hydrogen peroxide ; Life Sciences ; Male ; Medical Biochemistry ; Middle Aged ; Oncology ; Oxidative Stress ; Peroxiredoxins - genetics ; Peroxiredoxins - metabolism ; RNA ; Up-Regulation</subject><ispartof>Molecular and cellular biochemistry, 2014-02, Vol.387 (1-2), p.261-270</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>COPYRIGHT 2014 Springer</rights><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-de8388cc4f262bb2bed9dcb84e8e668ed6950dc03de616654267e60c9a6960f83</citedby><cites>FETCH-LOGICAL-c505t-de8388cc4f262bb2bed9dcb84e8e668ed6950dc03de616654267e60c9a6960f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-013-1891-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-013-1891-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24234423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Weidong</creatorcontrib><creatorcontrib>Fu, Zhongxue</creatorcontrib><creatorcontrib>Wang, Hao</creatorcontrib><creatorcontrib>Feng, Jihong</creatorcontrib><creatorcontrib>Wei, Jinlai</creatorcontrib><creatorcontrib>Guo, Jinbao</creatorcontrib><title>Peroxiredoxin 2 is upregulated in colorectal cancer and contributes to colorectal cancer cells’ survival by protecting cells from oxidative stress</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Peroxiredoxin 2 (Prdx2) is a member of the peroxiredoxin family, which is responsible for neutralizing reactive oxygen species. Prdx2 has been found to be elevated in several human cancer cells and tissues, including colorectal cancer (CRC), and it influences diverse cellular processes involving cells’ survival, proliferation, and apoptosis, which suggests a possible role for Prdx2 in the maintenance of cancer cell. However, the mechanism by which Prdx2 modulates CRC cells’ survival is unknown. The current study aimed to determine the effect of elevated Prdx2 on CRC cells and to further understand the underlying mechanisms. The results of this study showed that Prdx2 was upregulated in CRC tissues compared with the matched noncancer colorectal mucosa tissues and that Prdx2 expression was positively associated with tumor metastasis and the TNM stage. In the LoVo CRC cell line, Prdx2 was upregulated at both the RNA and protein levels compared with the normal FHC colorectal mucosa cell line. In addition, the LoVo CRC cell line was significantly more resistant to hydrogen peroxide (H
2
O
2
)-induced apoptosis because of a failure to activate pro-apoptotic pathways in contrast to Prdx2 knockdown cells. Suppression of Prdx2 using a lentiviral vector-mediated Prdx2-specific shRNA in the LoVo cell line restored H
2
O
2
sensitivity. Our results suggested that Prdx2 has an essential role in regulating oxidation-induced apoptosis in CRC cells. Prdx2 may have potential as a therapeutic target in CRC.</description><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - pathology</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer cells</subject><subject>Cardiology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Cellular biology</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - enzymology</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Disease Progression</subject><subject>Enzymes</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Middle Aged</subject><subject>Oncology</subject><subject>Oxidative Stress</subject><subject>Peroxiredoxins - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Weidong</au><au>Fu, Zhongxue</au><au>Wang, Hao</au><au>Feng, Jihong</au><au>Wei, Jinlai</au><au>Guo, Jinbao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxiredoxin 2 is upregulated in colorectal cancer and contributes to colorectal cancer cells’ survival by protecting cells from oxidative stress</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>387</volume><issue>1-2</issue><spage>261</spage><epage>270</epage><pages>261-270</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Peroxiredoxin 2 (Prdx2) is a member of the peroxiredoxin family, which is responsible for neutralizing reactive oxygen species. Prdx2 has been found to be elevated in several human cancer cells and tissues, including colorectal cancer (CRC), and it influences diverse cellular processes involving cells’ survival, proliferation, and apoptosis, which suggests a possible role for Prdx2 in the maintenance of cancer cell. However, the mechanism by which Prdx2 modulates CRC cells’ survival is unknown. The current study aimed to determine the effect of elevated Prdx2 on CRC cells and to further understand the underlying mechanisms. The results of this study showed that Prdx2 was upregulated in CRC tissues compared with the matched noncancer colorectal mucosa tissues and that Prdx2 expression was positively associated with tumor metastasis and the TNM stage. In the LoVo CRC cell line, Prdx2 was upregulated at both the RNA and protein levels compared with the normal FHC colorectal mucosa cell line. In addition, the LoVo CRC cell line was significantly more resistant to hydrogen peroxide (H
2
O
2
)-induced apoptosis because of a failure to activate pro-apoptotic pathways in contrast to Prdx2 knockdown cells. Suppression of Prdx2 using a lentiviral vector-mediated Prdx2-specific shRNA in the LoVo cell line restored H
2
O
2
sensitivity. Our results suggested that Prdx2 has an essential role in regulating oxidation-induced apoptosis in CRC cells. Prdx2 may have potential as a therapeutic target in CRC.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24234423</pmid><doi>10.1007/s11010-013-1891-4</doi><tpages>10</tpages></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2014-02, Vol.387 (1-2), p.261-270 |
| issn | 0300-8177 1573-4919 |
| language | eng |
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| subjects | Adenocarcinoma - enzymology Adenocarcinoma - pathology Apoptosis Biochemistry Biomedical and Life Sciences Cancer cells Cardiology Cell Line, Tumor Cell Survival Cellular biology Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - enzymology Colorectal Neoplasms - pathology Disease Progression Enzymes Female Gene Expression Health aspects Humans Hydrogen peroxide Life Sciences Male Medical Biochemistry Middle Aged Oncology Oxidative Stress Peroxiredoxins - genetics Peroxiredoxins - metabolism RNA Up-Regulation |
| title | Peroxiredoxin 2 is upregulated in colorectal cancer and contributes to colorectal cancer cells’ survival by protecting cells from oxidative stress |
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