Overexpression of NAC1 confers drug resistance via HOXA9 in colorectal carcinoma cells
Colorectal carcinoma (CRC) is one of the most common types of malignancy worldwide. Recently, neoadjuvant chemotherapy has become an important treatment strategy for CRC. However, treatment frequently fails due to the development of chemoresistance, which is a major obstacle for positive prognosis....
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| Veröffentlicht in: | Molecular medicine reports 2017-09, Vol.16 (3), p.3194-3200 |
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| description | Colorectal carcinoma (CRC) is one of the most common types of malignancy worldwide. Recently, neoadjuvant chemotherapy has become an important treatment strategy for CRC. However, treatment frequently fails due to the development of chemoresistance, which is a major obstacle for positive prognosis. However, the underlying mechanisms of chemoresistance remain unclear. The present study assessed the functions of nucleus accumbens-associated protein 1 (NAC1), an important transcriptional regulator, in CRC progression. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were performed to detect the expression levels of NAC1. It was identified that NAC1 was significantly overexpressed in CRC compared with non-tumorous tissues, indicating an oncogenic role. Following this, gain and loss of function analyses were performed in vitro to further investigate the function of NAC1. Cell viability and caspase-3/7 activity assays were used to assess chemotherapy-induced apoptosis. These results indicated that overexpression of NAC1 in CRC cells increased resistance to chemotherapy and inhibited apoptosis. Additionally, RNA interference-mediated knockdown of NAC1 restored the chemosensitivity of CRC cells. Furthermore, mechanistic investigation revealed that NAC1 increased drug resistance via inducing homeobox A9 (HOXA9) expression, and that knockdown of HOXA9 abrogated NAC1-induced drug resistance. In conclusion, the results of the present study demonstrated that NAC1 may be a critical factor in the development of chemoresistance, offering a potential novel target for the treatment of CRC. |
| doi_str_mv | 10.3892/mmr.2017.6986 |
| format | Article |
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Recently, neoadjuvant chemotherapy has become an important treatment strategy for CRC. However, treatment frequently fails due to the development of chemoresistance, which is a major obstacle for positive prognosis. However, the underlying mechanisms of chemoresistance remain unclear. The present study assessed the functions of nucleus accumbens-associated protein 1 (NAC1), an important transcriptional regulator, in CRC progression. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were performed to detect the expression levels of NAC1. It was identified that NAC1 was significantly overexpressed in CRC compared with non-tumorous tissues, indicating an oncogenic role. Following this, gain and loss of function analyses were performed in vitro to further investigate the function of NAC1. Cell viability and caspase-3/7 activity assays were used to assess chemotherapy-induced apoptosis. These results indicated that overexpression of NAC1 in CRC cells increased resistance to chemotherapy and inhibited apoptosis. Additionally, RNA interference-mediated knockdown of NAC1 restored the chemosensitivity of CRC cells. Furthermore, mechanistic investigation revealed that NAC1 increased drug resistance via inducing homeobox A9 (HOXA9) expression, and that knockdown of HOXA9 abrogated NAC1-induced drug resistance. In conclusion, the results of the present study demonstrated that NAC1 may be a critical factor in the development of chemoresistance, offering a potential novel target for the treatment of CRC.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6986</identifier><identifier>PMID: 28713930</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Autophagy ; Biotechnology ; Cancer therapies ; Care and treatment ; Caspase ; Caspase-3 ; Cell Line, Tumor ; Chemoresistance ; Chemotherapy ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Development and progression ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Fibroblasts ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes ; Genetic aspects ; Health aspects ; HEK293 Cells ; Homeobox ; homeobox A9 ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Immunohistochemistry ; Investigations ; Leukemia ; Malignancy ; Metastasis ; Motility ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Nucleus accumbens ; nucleus accumbens-associated protein 1 ; Ovarian cancer ; Polymerase chain reaction ; Proteins ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse transcription ; RNA-mediated interference ; Roles ; Senescence ; Surgery ; Transcription factors ; Tumors ; Up-Regulation - genetics</subject><ispartof>Molecular medicine reports, 2017-09, Vol.16 (3), p.3194-3200</ispartof><rights>Copyright: © Ju et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Ju et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-113c3a7747af367a1d76b7ffb3f795d68a6858f8d288a9da1732b26988e35eae3</citedby><cites>FETCH-LOGICAL-c580t-113c3a7747af367a1d76b7ffb3f795d68a6858f8d288a9da1732b26988e35eae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,5556,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28713930$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ju, Tongfa</creatorcontrib><creatorcontrib>Jin, Huicheng</creatorcontrib><creatorcontrib>Ying, Rongchao</creatorcontrib><creatorcontrib>Xie, Qi</creatorcontrib><creatorcontrib>Zhou, Chunhua</creatorcontrib><creatorcontrib>Gao, Daquan</creatorcontrib><title>Overexpression of NAC1 confers drug resistance via HOXA9 in colorectal carcinoma cells</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Colorectal carcinoma (CRC) is one of the most common types of malignancy worldwide. Recently, neoadjuvant chemotherapy has become an important treatment strategy for CRC. However, treatment frequently fails due to the development of chemoresistance, which is a major obstacle for positive prognosis. However, the underlying mechanisms of chemoresistance remain unclear. The present study assessed the functions of nucleus accumbens-associated protein 1 (NAC1), an important transcriptional regulator, in CRC progression. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were performed to detect the expression levels of NAC1. It was identified that NAC1 was significantly overexpressed in CRC compared with non-tumorous tissues, indicating an oncogenic role. Following this, gain and loss of function analyses were performed in vitro to further investigate the function of NAC1. Cell viability and caspase-3/7 activity assays were used to assess chemotherapy-induced apoptosis. These results indicated that overexpression of NAC1 in CRC cells increased resistance to chemotherapy and inhibited apoptosis. Additionally, RNA interference-mediated knockdown of NAC1 restored the chemosensitivity of CRC cells. Furthermore, mechanistic investigation revealed that NAC1 increased drug resistance via inducing homeobox A9 (HOXA9) expression, and that knockdown of HOXA9 abrogated NAC1-induced drug resistance. In conclusion, the results of the present study demonstrated that NAC1 may be a critical factor in the development of chemoresistance, offering a potential novel target for the treatment of CRC.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biotechnology</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell Line, Tumor</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Development and progression</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>HEK293 Cells</subject><subject>Homeobox</subject><subject>homeobox A9</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Investigations</subject><subject>Leukemia</subject><subject>Malignancy</subject><subject>Metastasis</subject><subject>Motility</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nucleus accumbens</subject><subject>nucleus accumbens-associated protein 1</subject><subject>Ovarian cancer</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse transcription</subject><subject>RNA-mediated interference</subject><subject>Roles</subject><subject>Senescence</subject><subject>Surgery</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Up-Regulation - genetics</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNptks2LEzEYxgdR3HX16FUCHtbL1HxMvi5CKeoKi72oeAtp5k3NMpPUpFP0vzdDa3VFckjI-3uf8Dx5m-Y5wQumNH09jnlBMZELoZV40FwSqUnLMO4ens5Ua3nRPCnlDmPBKdePmwuqJGGa4cvmy_oAGX7sMpQSUkTJo4_LFUEuRQ-5oD5PW1SLoextdIAOwaKb9delRiFWaEgZ3N4OyNnsQkyjRQ6GoTxtHnk7FHh22q-az-_eflrdtLfr9x9Wy9vWcYX3LSHMMStlJ61nQlrSS7GR3m-Yl5r3QlmhuPKqp0pZ3VsiGd3Q6lQB42CBXTVvjrq7aTNC7yDusx3MLofR5p8m2WDuV2L4ZrbpYDjvpBa4Crw6CeT0fYKyN2MoswUbIU3FEF3DrcnyGX35D3qXphyrvUp1lHCsuPhDbe0AJkSf6rtuFjVLToiQVPOuUov_UHX1MIaaPfhQ7-81tMcGl1MpGfzZI8FmHgRTB8HMg2DmQaj8i7-DOdO_f74C10eg7GzsQ5_KmalKLREtZi2rxtgvDAO6Jg</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Ju, Tongfa</creator><creator>Jin, Huicheng</creator><creator>Ying, Rongchao</creator><creator>Xie, Qi</creator><creator>Zhou, Chunhua</creator><creator>Gao, Daquan</creator><general>D.A. 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genetics</topic><topic>Development and progression</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Fibroblasts</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>HEK293 Cells</topic><topic>Homeobox</topic><topic>homeobox A9</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Investigations</topic><topic>Leukemia</topic><topic>Malignancy</topic><topic>Metastasis</topic><topic>Motility</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Nucleus accumbens</topic><topic>nucleus accumbens-associated protein 1</topic><topic>Ovarian cancer</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Repressor Proteins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ju, Tongfa</au><au>Jin, Huicheng</au><au>Ying, Rongchao</au><au>Xie, Qi</au><au>Zhou, Chunhua</au><au>Gao, Daquan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of NAC1 confers drug resistance via HOXA9 in colorectal carcinoma cells</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>16</volume><issue>3</issue><spage>3194</spage><epage>3200</epage><pages>3194-3200</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Colorectal carcinoma (CRC) is one of the most common types of malignancy worldwide. Recently, neoadjuvant chemotherapy has become an important treatment strategy for CRC. However, treatment frequently fails due to the development of chemoresistance, which is a major obstacle for positive prognosis. However, the underlying mechanisms of chemoresistance remain unclear. The present study assessed the functions of nucleus accumbens-associated protein 1 (NAC1), an important transcriptional regulator, in CRC progression. Reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry were performed to detect the expression levels of NAC1. It was identified that NAC1 was significantly overexpressed in CRC compared with non-tumorous tissues, indicating an oncogenic role. Following this, gain and loss of function analyses were performed in vitro to further investigate the function of NAC1. Cell viability and caspase-3/7 activity assays were used to assess chemotherapy-induced apoptosis. These results indicated that overexpression of NAC1 in CRC cells increased resistance to chemotherapy and inhibited apoptosis. Additionally, RNA interference-mediated knockdown of NAC1 restored the chemosensitivity of CRC cells. Furthermore, mechanistic investigation revealed that NAC1 increased drug resistance via inducing homeobox A9 (HOXA9) expression, and that knockdown of HOXA9 abrogated NAC1-induced drug resistance. In conclusion, the results of the present study demonstrated that NAC1 may be a critical factor in the development of chemoresistance, offering a potential novel target for the treatment of CRC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28713930</pmid><doi>10.3892/mmr.2017.6986</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Autophagy Biotechnology Cancer therapies Care and treatment Caspase Caspase-3 Cell Line, Tumor Chemoresistance Chemotherapy Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Development and progression Drug resistance Drug Resistance, Neoplasm - genetics Fibroblasts Gene expression Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Genes Genetic aspects Health aspects HEK293 Cells Homeobox homeobox A9 Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Immunohistochemistry Investigations Leukemia Malignancy Metastasis Motility Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Nucleus accumbens nucleus accumbens-associated protein 1 Ovarian cancer Polymerase chain reaction Proteins Repressor Proteins - genetics Repressor Proteins - metabolism Reverse transcription RNA-mediated interference Roles Senescence Surgery Transcription factors Tumors Up-Regulation - genetics |
| title | Overexpression of NAC1 confers drug resistance via HOXA9 in colorectal carcinoma cells |
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