Mitochondrial Ca2+ uniporter is critical for store-operated Ca2+ entry-dependent breast cancer cell migration
Metastasis of cancer cells is a complicated multistep process requiring extensive and continuous cytosolic calcium modulation. Mitochondrial Ca2+ uniporter (MCU), a regulator of mitochondrial Ca2+ uptake, has been implicated in energy metabolism and various cellular signaling processes. However, whe...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2015-02, Vol.458 (1), p.186-193 |
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| creator | Tang, Shihao Wang, Xubu Shen, Qiang Yang, Xinyi Yu, Changhui Cai, Chunqing Cai, Guoshuai Meng, Xiaojing Zou, Fei |
| description | Metastasis of cancer cells is a complicated multistep process requiring extensive and continuous cytosolic calcium modulation. Mitochondrial Ca2+ uniporter (MCU), a regulator of mitochondrial Ca2+ uptake, has been implicated in energy metabolism and various cellular signaling processes. However, whether MCU contributes to cancer cell migration has not been established. Here we examined the expression of MCU mRNA in the Oncomine database and found that MCU is correlated to metastasis and invasive breast cancer. MCU inhibition by ruthenium red (RuR) or MCU silencing by siRNA abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or thapsigargin (TG)-induced store-operated Ca2+ entry (SOCE). Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors. Our results demonstrate that MCU plays a critical role in breast cancer cell migration by regulating SOCE.
•MCU is correlated to metastasis and invasive breast cancer.•MCU inhibition abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or TG-induced SOCE.•Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors.•MCU plays a critical role in MDA-MB-231 cell migration by regulating SOCE. |
| doi_str_mv | 10.1016/j.bbrc.2015.01.092 |
| format | Article |
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•MCU is correlated to metastasis and invasive breast cancer.•MCU inhibition abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or TG-induced SOCE.•Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors.•MCU plays a critical role in MDA-MB-231 cell migration by regulating SOCE.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2015.01.092</identifier><identifier>PMID: 25640838</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Breast tumor ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium Channels - genetics ; Calcium Channels - metabolism ; Cell Line, Tumor ; Cell Movement - drug effects ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Imidazoles - pharmacology ; MCU ; Migration ; Mitochondria - drug effects ; Mitochondria - metabolism ; Ruthenium Red - pharmacology ; SOCE ; Thapsigargin - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2015-02, Vol.458 (1), p.186-193</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c319t-1bc167e437c56160acaf0b60aad298248ad86dd6b27c73617c74813e1a4d7e703</citedby><cites>FETCH-LOGICAL-c319t-1bc167e437c56160acaf0b60aad298248ad86dd6b27c73617c74813e1a4d7e703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X1500131X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25640838$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Shihao</creatorcontrib><creatorcontrib>Wang, Xubu</creatorcontrib><creatorcontrib>Shen, Qiang</creatorcontrib><creatorcontrib>Yang, Xinyi</creatorcontrib><creatorcontrib>Yu, Changhui</creatorcontrib><creatorcontrib>Cai, Chunqing</creatorcontrib><creatorcontrib>Cai, Guoshuai</creatorcontrib><creatorcontrib>Meng, Xiaojing</creatorcontrib><creatorcontrib>Zou, Fei</creatorcontrib><title>Mitochondrial Ca2+ uniporter is critical for store-operated Ca2+ entry-dependent breast cancer cell migration</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Metastasis of cancer cells is a complicated multistep process requiring extensive and continuous cytosolic calcium modulation. Mitochondrial Ca2+ uniporter (MCU), a regulator of mitochondrial Ca2+ uptake, has been implicated in energy metabolism and various cellular signaling processes. However, whether MCU contributes to cancer cell migration has not been established. Here we examined the expression of MCU mRNA in the Oncomine database and found that MCU is correlated to metastasis and invasive breast cancer. MCU inhibition by ruthenium red (RuR) or MCU silencing by siRNA abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or thapsigargin (TG)-induced store-operated Ca2+ entry (SOCE). Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors. Our results demonstrate that MCU plays a critical role in breast cancer cell migration by regulating SOCE.
•MCU is correlated to metastasis and invasive breast cancer.•MCU inhibition abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or TG-induced SOCE.•Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors.•MCU plays a critical role in MDA-MB-231 cell migration by regulating SOCE.</description><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast tumor</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels - genetics</subject><subject>Calcium Channels - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Imidazoles - pharmacology</subject><subject>MCU</subject><subject>Migration</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Ruthenium Red - pharmacology</subject><subject>SOCE</subject><subject>Thapsigargin - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2r1DAUhoMo3vHqH3AhXQrSek7aJi24kcEvuOJGwV1IkzOaYdrUk8yF--9NmatL3eQE8r4P4TxCPEdoEFC9PjbTxK6RgH0D2MAoH4gdwgi1ROgeih0AqFqO-P1KPEnpCIDYqfGxuJK96mBoh52YP4cc3c-4eA72VO2tfFWdl7BGzsRVSJXjkIMrT4fIVcqRqY4rsc3kL2laMt_VnlZafLlXE5NNuXJ2cYXg6HSq5vCjFEJcnopHB3tK9Ox-Xotv79993X-sb758-LR_e1O7Fsdc4-RQaepa7XqFCqyzB5jKtF6Og-wG6wflvZqkdrpVWM5uwJbQdl6ThvZavLxwV46_zpSymUPavmIXiudkUAN2Wsmx_39U9bqVuh03qrxEHceUmA5m5TBbvjMIZjNijmYzYjYjBtAUI6X04p5_nmbyfyt_FJTAm0uAykJuA7FJLlBZng9MLhsfw7_4vwE9kJxz</recordid><startdate>20150227</startdate><enddate>20150227</enddate><creator>Tang, Shihao</creator><creator>Wang, Xubu</creator><creator>Shen, Qiang</creator><creator>Yang, Xinyi</creator><creator>Yu, Changhui</creator><creator>Cai, Chunqing</creator><creator>Cai, Guoshuai</creator><creator>Meng, Xiaojing</creator><creator>Zou, Fei</creator><general>Elsevier Inc</general><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>7X8</scope><scope>7QP</scope></search><sort><creationdate>20150227</creationdate><title>Mitochondrial Ca2+ uniporter is critical for store-operated Ca2+ entry-dependent breast cancer cell migration</title><author>Tang, Shihao ; Wang, Xubu ; Shen, Qiang ; Yang, Xinyi ; Yu, Changhui ; Cai, Chunqing ; Cai, Guoshuai ; Meng, Xiaojing ; Zou, Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c319t-1bc167e437c56160acaf0b60aad298248ad86dd6b27c73617c74813e1a4d7e703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast tumor</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels - genetics</topic><topic>Calcium Channels - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Imidazoles - pharmacology</topic><topic>MCU</topic><topic>Migration</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Ruthenium Red - pharmacology</topic><topic>SOCE</topic><topic>Thapsigargin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Shihao</creatorcontrib><creatorcontrib>Wang, Xubu</creatorcontrib><creatorcontrib>Shen, Qiang</creatorcontrib><creatorcontrib>Yang, Xinyi</creatorcontrib><creatorcontrib>Yu, Changhui</creatorcontrib><creatorcontrib>Cai, Chunqing</creatorcontrib><creatorcontrib>Cai, Guoshuai</creatorcontrib><creatorcontrib>Meng, Xiaojing</creatorcontrib><creatorcontrib>Zou, Fei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Calcium & Calcified Tissue Abstracts</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Shihao</au><au>Wang, Xubu</au><au>Shen, Qiang</au><au>Yang, Xinyi</au><au>Yu, Changhui</au><au>Cai, Chunqing</au><au>Cai, Guoshuai</au><au>Meng, Xiaojing</au><au>Zou, Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial Ca2+ uniporter is critical for store-operated Ca2+ entry-dependent breast cancer cell migration</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2015-02-27</date><risdate>2015</risdate><volume>458</volume><issue>1</issue><spage>186</spage><epage>193</epage><pages>186-193</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Metastasis of cancer cells is a complicated multistep process requiring extensive and continuous cytosolic calcium modulation. Mitochondrial Ca2+ uniporter (MCU), a regulator of mitochondrial Ca2+ uptake, has been implicated in energy metabolism and various cellular signaling processes. However, whether MCU contributes to cancer cell migration has not been established. Here we examined the expression of MCU mRNA in the Oncomine database and found that MCU is correlated to metastasis and invasive breast cancer. MCU inhibition by ruthenium red (RuR) or MCU silencing by siRNA abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or thapsigargin (TG)-induced store-operated Ca2+ entry (SOCE). Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors. Our results demonstrate that MCU plays a critical role in breast cancer cell migration by regulating SOCE.
•MCU is correlated to metastasis and invasive breast cancer.•MCU inhibition abolished serum-induced migration in MDA-MB-231 breast cancer cells and reduced serum- or TG-induced SOCE.•Serum-induced migrations in MDA-MB-231 cells were blocked by SOCE inhibitors.•MCU plays a critical role in MDA-MB-231 cell migration by regulating SOCE.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25640838</pmid><doi>10.1016/j.bbrc.2015.01.092</doi><tpages>8</tpages></addata></record> |
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| subjects | Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Breast tumor Calcium - metabolism Calcium Channel Blockers - pharmacology Calcium Channels - genetics Calcium Channels - metabolism Cell Line, Tumor Cell Movement - drug effects Female Gene Expression Regulation, Neoplastic Humans Imidazoles - pharmacology MCU Migration Mitochondria - drug effects Mitochondria - metabolism Ruthenium Red - pharmacology SOCE Thapsigargin - pharmacology |
| title | Mitochondrial Ca2+ uniporter is critical for store-operated Ca2+ entry-dependent breast cancer cell migration |
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