Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14
Background/Aims: Osterix (Osx), a key regulator of osteoblast differentiation and bone formation, has been recently reported to be associated with the progression of breast cancer. However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was as...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2017-01, Vol.44 (3), p.998-1010 |
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| creator | Wu, Jiahui Chen, Xiang Bao, Qianyi Duan, Rui Jin, Yucui Shui, Yifang Yao, Bing Lu, Xiangdong Wang, Yue Cui, Hongyan Li, Lingyun Yuan, Hongyan Ma, Changyan |
| description | Background/Aims: Osterix (Osx), a key regulator of osteoblast differentiation and bone formation, has been recently reported to be associated with the progression of breast cancer. However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was assessed using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Target genes were obtained by high-throughput Illumina sequencing and were confirmed in vitro and in vivo. Apoptosis was analysed by Hoechst staining and western blotting. A tissue microarray including 129 samples from breast cancer patients was used for immunohistochemistry (IHC) assays. Results: Overexpression of Osx decreased the chemosensitivity of breast cancer cells, while knockdown of Osx increased the chemosensitivity of breast cancer cells. In particular, we found that the decreased chemosensitivity effect was significantly associated with elevated expression of the polypeptide N-acetylgalactosaminyltransferase 14 (GALNT14). Silencing of GALNT14 in Osx-overexpressed cells restored the decreased chemosensitivity. Conversely, overexpression of GALNT14 in Osx-knockdown cells abrogated the increased chemosensitivity in breast cancer cells. In addition, we revealed that Osx decreased GALNT14-dependent chemosensitivity by enhancing anti-apoptosis. GALNT14 expression exhibited a significant association with breast cancer stages as well as the disease-free survival (DFS) rate. Conclusion: Osx plays an important role in the chemosensitivity and inhibition of Osx expression may represent a therapeutic strategy to enhance the chemosensitivity of breast cancer. |
| doi_str_mv | 10.1159/000485400 |
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However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was assessed using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Target genes were obtained by high-throughput Illumina sequencing and were confirmed in vitro and in vivo. Apoptosis was analysed by Hoechst staining and western blotting. A tissue microarray including 129 samples from breast cancer patients was used for immunohistochemistry (IHC) assays. Results: Overexpression of Osx decreased the chemosensitivity of breast cancer cells, while knockdown of Osx increased the chemosensitivity of breast cancer cells. In particular, we found that the decreased chemosensitivity effect was significantly associated with elevated expression of the polypeptide N-acetylgalactosaminyltransferase 14 (GALNT14). Silencing of GALNT14 in Osx-overexpressed cells restored the decreased chemosensitivity. Conversely, overexpression of GALNT14 in Osx-knockdown cells abrogated the increased chemosensitivity in breast cancer cells. In addition, we revealed that Osx decreased GALNT14-dependent chemosensitivity by enhancing anti-apoptosis. GALNT14 expression exhibited a significant association with breast cancer stages as well as the disease-free survival (DFS) rate. Conclusion: Osx plays an important role in the chemosensitivity and inhibition of Osx expression may represent a therapeutic strategy to enhance the chemosensitivity of breast cancer.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000485400</identifier><identifier>PMID: 29227978</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Antineoplastic Agents - therapeutic use ; Antineoplastic Agents - toxicity ; Apoptosis - drug effects ; bcl-2-Associated X Protein - metabolism ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - mortality ; Breast Neoplasms - pathology ; Cancer cells ; Cancer therapies ; Cell Line, Tumor ; Chemosensitivity ; Chemotherapy ; Disease-Free Survival ; Female ; GALNT14 ; Health aspects ; Humans ; Immunoglobulins ; Immunohistochemistry ; Liver cancer ; Lung cancer ; Medical prognosis ; Mice ; Mice, Nude ; N-Acetylgalactosaminyltransferases - antagonists & inhibitors ; N-Acetylgalactosaminyltransferases - genetics ; N-Acetylgalactosaminyltransferases - metabolism ; Original Paper ; Osterix ; Ovarian cancer ; Physiological aspects ; Polypeptides ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; Sp7 Transcription Factor - antagonists & inhibitors ; Sp7 Transcription Factor - genetics ; Sp7 Transcription Factor - metabolism ; Survival Rate ; Transplantation, Heterologous</subject><ispartof>Cellular Physiology and Biochemistry, 2017-01, Vol.44 (3), p.998-1010</ispartof><rights>2017 The Author(s). Published by S. Karger AG, Basel</rights><rights>2017 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2017 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c530t-d28ff7cc98606258d889e4ad38852f3bf1c02eebbcb8620e03b61847d1e83f763</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29227978$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Jiahui</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Bao, Qianyi</creatorcontrib><creatorcontrib>Duan, Rui</creatorcontrib><creatorcontrib>Jin, Yucui</creatorcontrib><creatorcontrib>Shui, Yifang</creatorcontrib><creatorcontrib>Yao, Bing</creatorcontrib><creatorcontrib>Lu, Xiangdong</creatorcontrib><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Cui, Hongyan</creatorcontrib><creatorcontrib>Li, Lingyun</creatorcontrib><creatorcontrib>Yuan, Hongyan</creatorcontrib><creatorcontrib>Ma, Changyan</creatorcontrib><title>Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Osterix (Osx), a key regulator of osteoblast differentiation and bone formation, has been recently reported to be associated with the progression of breast cancer. However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was assessed using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Target genes were obtained by high-throughput Illumina sequencing and were confirmed in vitro and in vivo. Apoptosis was analysed by Hoechst staining and western blotting. A tissue microarray including 129 samples from breast cancer patients was used for immunohistochemistry (IHC) assays. Results: Overexpression of Osx decreased the chemosensitivity of breast cancer cells, while knockdown of Osx increased the chemosensitivity of breast cancer cells. In particular, we found that the decreased chemosensitivity effect was significantly associated with elevated expression of the polypeptide N-acetylgalactosaminyltransferase 14 (GALNT14). Silencing of GALNT14 in Osx-overexpressed cells restored the decreased chemosensitivity. Conversely, overexpression of GALNT14 in Osx-knockdown cells abrogated the increased chemosensitivity in breast cancer cells. In addition, we revealed that Osx decreased GALNT14-dependent chemosensitivity by enhancing anti-apoptosis. GALNT14 expression exhibited a significant association with breast cancer stages as well as the disease-free survival (DFS) rate. Conclusion: Osx plays an important role in the chemosensitivity and inhibition of Osx expression may represent a therapeutic strategy to enhance the chemosensitivity of breast cancer.</description><subject>Animals</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic Agents - toxicity</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - mortality</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Chemosensitivity</subject><subject>Chemotherapy</subject><subject>Disease-Free Survival</subject><subject>Female</subject><subject>GALNT14</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Immunohistochemistry</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>N-Acetylgalactosaminyltransferases - antagonists & inhibitors</subject><subject>N-Acetylgalactosaminyltransferases - genetics</subject><subject>N-Acetylgalactosaminyltransferases - metabolism</subject><subject>Original Paper</subject><subject>Osterix</subject><subject>Ovarian cancer</subject><subject>Physiological aspects</subject><subject>Polypeptides</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Sp7 Transcription Factor - antagonists & inhibitors</subject><subject>Sp7 Transcription Factor - genetics</subject><subject>Sp7 Transcription Factor - metabolism</subject><subject>Survival Rate</subject><subject>Transplantation, Heterologous</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkc1v1DAUxC0EomXhwB0hSz1xSPFXYue4DbRUWlEO3bPlOM-pl2y82FnE_ve4TckJ-WD7vd-MRhqE3lNySWlZfyaECFUKQl6gcyoYLWop1cv8JrQsVK3kGXqT0o7kr6zZa3TGasZkLdU52t6lCaL_g7-AjWASJDw9AG4eYB8SjMlP_refTjg4fPW4n3BjRgsRNzAMCbcnvD1E6I-DmfzY45v15vs9FW_RK2eGBO-e7xXaXn-9b74Vm7ub22a9KWzJyVR0TDknra1VRSpWqk6pGoTpuFIlc7x11BIG0La2VRUjQHhbUSVkR0FxJyu-QrezbxfMTh-i35t40sF4_TQIsdcmTt4OoB2rZFV2rTSuFLTmrVTEUG6YEIpVOc8KXcxehxh-HSFNeheOcczxNaNUUlExRjN1OVO9yaZ-dGGKxubTwd7bMILzeb6uuCwZI5RnwadZYGNIKYJbYlKiH9vTS3uZ_fgc4djuoVvIf3Vl4MMM_DSxh7gAi_7iv-vmx9VM6EPn-F_qvaY3</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Wu, Jiahui</creator><creator>Chen, Xiang</creator><creator>Bao, Qianyi</creator><creator>Duan, Rui</creator><creator>Jin, Yucui</creator><creator>Shui, Yifang</creator><creator>Yao, Bing</creator><creator>Lu, Xiangdong</creator><creator>Wang, Yue</creator><creator>Cui, Hongyan</creator><creator>Li, Lingyun</creator><creator>Yuan, Hongyan</creator><creator>Ma, Changyan</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>IAO</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>DOA</scope></search><sort><creationdate>20170101</creationdate><title>Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14</title><author>Wu, Jiahui ; Chen, Xiang ; Bao, Qianyi ; Duan, Rui ; Jin, Yucui ; Shui, Yifang ; Yao, Bing ; Lu, Xiangdong ; Wang, Yue ; Cui, Hongyan ; Li, Lingyun ; Yuan, Hongyan ; Ma, Changyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-d28ff7cc98606258d889e4ad38852f3bf1c02eebbcb8620e03b61847d1e83f763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antineoplastic Agents - toxicity</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - mortality</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Cell Line, Tumor</topic><topic>Chemosensitivity</topic><topic>Chemotherapy</topic><topic>Disease-Free Survival</topic><topic>Female</topic><topic>GALNT14</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Immunohistochemistry</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>N-Acetylgalactosaminyltransferases - antagonists & inhibitors</topic><topic>N-Acetylgalactosaminyltransferases - genetics</topic><topic>N-Acetylgalactosaminyltransferases - metabolism</topic><topic>Original Paper</topic><topic>Osterix</topic><topic>Ovarian cancer</topic><topic>Physiological aspects</topic><topic>Polypeptides</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Sp7 Transcription Factor - antagonists & inhibitors</topic><topic>Sp7 Transcription Factor - genetics</topic><topic>Sp7 Transcription Factor - metabolism</topic><topic>Survival Rate</topic><topic>Transplantation, Heterologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Jiahui</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Bao, Qianyi</creatorcontrib><creatorcontrib>Duan, Rui</creatorcontrib><creatorcontrib>Jin, Yucui</creatorcontrib><creatorcontrib>Shui, Yifang</creatorcontrib><creatorcontrib>Yao, Bing</creatorcontrib><creatorcontrib>Lu, Xiangdong</creatorcontrib><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Cui, Hongyan</creatorcontrib><creatorcontrib>Li, Lingyun</creatorcontrib><creatorcontrib>Yuan, Hongyan</creatorcontrib><creatorcontrib>Ma, Changyan</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Jiahui</au><au>Chen, Xiang</au><au>Bao, Qianyi</au><au>Duan, Rui</au><au>Jin, Yucui</au><au>Shui, Yifang</au><au>Yao, Bing</au><au>Lu, Xiangdong</au><au>Wang, Yue</au><au>Cui, Hongyan</au><au>Li, Lingyun</au><au>Yuan, Hongyan</au><au>Ma, Changyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>44</volume><issue>3</issue><spage>998</spage><epage>1010</epage><pages>998-1010</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Osterix (Osx), a key regulator of osteoblast differentiation and bone formation, has been recently reported to be associated with the progression of breast cancer. However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was assessed using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Target genes were obtained by high-throughput Illumina sequencing and were confirmed in vitro and in vivo. Apoptosis was analysed by Hoechst staining and western blotting. A tissue microarray including 129 samples from breast cancer patients was used for immunohistochemistry (IHC) assays. Results: Overexpression of Osx decreased the chemosensitivity of breast cancer cells, while knockdown of Osx increased the chemosensitivity of breast cancer cells. In particular, we found that the decreased chemosensitivity effect was significantly associated with elevated expression of the polypeptide N-acetylgalactosaminyltransferase 14 (GALNT14). Silencing of GALNT14 in Osx-overexpressed cells restored the decreased chemosensitivity. Conversely, overexpression of GALNT14 in Osx-knockdown cells abrogated the increased chemosensitivity in breast cancer cells. In addition, we revealed that Osx decreased GALNT14-dependent chemosensitivity by enhancing anti-apoptosis. GALNT14 expression exhibited a significant association with breast cancer stages as well as the disease-free survival (DFS) rate. Conclusion: Osx plays an important role in the chemosensitivity and inhibition of Osx expression may represent a therapeutic strategy to enhance the chemosensitivity of breast cancer.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29227978</pmid><doi>10.1159/000485400</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic Agents - therapeutic use Antineoplastic Agents - toxicity Apoptosis - drug effects bcl-2-Associated X Protein - metabolism Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - mortality Breast Neoplasms - pathology Cancer cells Cancer therapies Cell Line, Tumor Chemosensitivity Chemotherapy Disease-Free Survival Female GALNT14 Health aspects Humans Immunoglobulins Immunohistochemistry Liver cancer Lung cancer Medical prognosis Mice Mice, Nude N-Acetylgalactosaminyltransferases - antagonists & inhibitors N-Acetylgalactosaminyltransferases - genetics N-Acetylgalactosaminyltransferases - metabolism Original Paper Osterix Ovarian cancer Physiological aspects Polypeptides Proteins Proto-Oncogene Proteins c-bcl-2 - metabolism RNA Interference RNA, Small Interfering - metabolism Sp7 Transcription Factor - antagonists & inhibitors Sp7 Transcription Factor - genetics Sp7 Transcription Factor - metabolism Survival Rate Transplantation, Heterologous |
| title | Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14 |
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