Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells
Background FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied. Methods The expression of FAM64A mRNA in BrC samples was determined...
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| Veröffentlicht in: | Breast cancer (Tokyo, Japan) Japan), 2019-11, Vol.26 (6), p.835-845 |
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| container_title | Breast cancer (Tokyo, Japan) |
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| creator | Yao, Zhuocheng Zheng, Xianchong Lu, Sitong He, Zhanxin Miao, Yutian Huang, Hehai Chu, Xinwei Cai, Chunqing Zou, Fei |
| description | Background
FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.
Methods
The expression of
FAM64A
mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (
Snail
,
Twist
,
Slug
) were conducted to evaluate the migration ability.
Results
FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.
Conclusions
Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment. |
| doi_str_mv | 10.1007/s12282-019-00991-2 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_cross</sourceid><recordid>TN_cdi_gale_infotracmisc_A712280515</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A712280515</galeid><sourcerecordid>A712280515</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-eefab1387d0c80ccb15d9c732374779e43cc1225afad71ccbce14bae65625e6b3</originalsourceid><addsrcrecordid>eNp9kNtKxDAQhoMonl_ACyl4XZ0cmrSXi3hCRQS9Dmk6Xbq2SUl2Ed_erF0FQSQXk8z830A-Qk4onFMAdREpYyXLgVY5QFXRnG2RfVqWkAvG-Xa6cwG5LGW5Rw5iXAAIrkDukj1OmRSg5D55vnfevjX-3WW-za5nj1LMsrgax4AxYszG4PuuxWCWnXeZcU02dPPNKwF1QBOXmTXOYsgs9n08Ijut6SMeb-oheb2-erm8zR-ebu4uZw-5LUAsc8TW1JSXqgFbgrU1LZrKKs64EkpVKLi16X-FaU2jaJpbpKI2KAvJCpQ1PyRn09656VF3rvXLYOzQRatnam0GClqk1PkfqXQaHDrrHbZd6v8C2ATY4GMM2OoxdIMJH5qCXmvXk3adtOsv7Zol6HSCxlU9YPODfHtOAT4FYhq5OQa98Kvgkp__1n4C-v6Mtg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Yao, Zhuocheng ; Zheng, Xianchong ; Lu, Sitong ; He, Zhanxin ; Miao, Yutian ; Huang, Hehai ; Chu, Xinwei ; Cai, Chunqing ; Zou, Fei</creator><creatorcontrib>Yao, Zhuocheng ; Zheng, Xianchong ; Lu, Sitong ; He, Zhanxin ; Miao, Yutian ; Huang, Hehai ; Chu, Xinwei ; Cai, Chunqing ; Zou, Fei</creatorcontrib><description>Background
FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.
Methods
The expression of
FAM64A
mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (
Snail
,
Twist
,
Slug
) were conducted to evaluate the migration ability.
Results
FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.
Conclusions
Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment.</description><identifier>ISSN: 1340-6868</identifier><identifier>EISSN: 1880-4233</identifier><identifier>DOI: 10.1007/s12282-019-00991-2</identifier><identifier>PMID: 31264076</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Analysis ; Antigens, CD - metabolism ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cadherins - metabolism ; Cancer cells ; Cancer Research ; Cell Movement - genetics ; Cell Proliferation - genetics ; DNA binding proteins ; Epithelial-Mesenchymal Transition - genetics ; Female ; G1 Phase Cell Cycle Checkpoints - genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Kaplan-Meier Estimate ; MCF-7 Cells ; Medicine ; Medicine & Public Health ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncology ; Original Article ; Prognosis ; RNA ; RNA Interference ; Snail Family Transcription Factors - metabolism ; Surgery ; Surgical Oncology ; Transfection ; Twist-Related Protein 1 - metabolism ; Vimentin - metabolism</subject><ispartof>Breast cancer (Tokyo, Japan), 2019-11, Vol.26 (6), p.835-845</ispartof><rights>The Japanese Breast Cancer Society 2019</rights><rights>COPYRIGHT 2019 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-eefab1387d0c80ccb15d9c732374779e43cc1225afad71ccbce14bae65625e6b3</citedby><cites>FETCH-LOGICAL-c504t-eefab1387d0c80ccb15d9c732374779e43cc1225afad71ccbce14bae65625e6b3</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/s12282-019-00991-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12282-019-00991-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31264076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yao, Zhuocheng</creatorcontrib><creatorcontrib>Zheng, Xianchong</creatorcontrib><creatorcontrib>Lu, Sitong</creatorcontrib><creatorcontrib>He, Zhanxin</creatorcontrib><creatorcontrib>Miao, Yutian</creatorcontrib><creatorcontrib>Huang, Hehai</creatorcontrib><creatorcontrib>Chu, Xinwei</creatorcontrib><creatorcontrib>Cai, Chunqing</creatorcontrib><creatorcontrib>Zou, Fei</creatorcontrib><title>Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells</title><title>Breast cancer (Tokyo, Japan)</title><addtitle>Breast Cancer</addtitle><addtitle>Breast Cancer</addtitle><description>Background
FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.
Methods
The expression of
FAM64A
mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (
Snail
,
Twist
,
Slug
) were conducted to evaluate the migration ability.
Results
FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.
Conclusions
Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment.</description><subject>Analysis</subject><subject>Antigens, CD - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cadherins - metabolism</subject><subject>Cancer cells</subject><subject>Cancer Research</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>DNA binding proteins</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>G1 Phase Cell Cycle Checkpoints - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Kaplan-Meier Estimate</subject><subject>MCF-7 Cells</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Prognosis</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>Snail Family Transcription Factors - metabolism</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Transfection</subject><subject>Twist-Related Protein 1 - metabolism</subject><subject>Vimentin - metabolism</subject><issn>1340-6868</issn><issn>1880-4233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kNtKxDAQhoMonl_ACyl4XZ0cmrSXi3hCRQS9Dmk6Xbq2SUl2Ed_erF0FQSQXk8z830A-Qk4onFMAdREpYyXLgVY5QFXRnG2RfVqWkAvG-Xa6cwG5LGW5Rw5iXAAIrkDukj1OmRSg5D55vnfevjX-3WW-za5nj1LMsrgax4AxYszG4PuuxWCWnXeZcU02dPPNKwF1QBOXmTXOYsgs9n08Ijut6SMeb-oheb2-erm8zR-ebu4uZw-5LUAsc8TW1JSXqgFbgrU1LZrKKs64EkpVKLi16X-FaU2jaJpbpKI2KAvJCpQ1PyRn09656VF3rvXLYOzQRatnam0GClqk1PkfqXQaHDrrHbZd6v8C2ATY4GMM2OoxdIMJH5qCXmvXk3adtOsv7Zol6HSCxlU9YPODfHtOAT4FYhq5OQa98Kvgkp__1n4C-v6Mtg</recordid><startdate>20191101</startdate><enddate>20191101</enddate><creator>Yao, Zhuocheng</creator><creator>Zheng, Xianchong</creator><creator>Lu, Sitong</creator><creator>He, Zhanxin</creator><creator>Miao, Yutian</creator><creator>Huang, Hehai</creator><creator>Chu, Xinwei</creator><creator>Cai, Chunqing</creator><creator>Zou, Fei</creator><general>Springer Japan</general><general>Springer</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></search><sort><creationdate>20191101</creationdate><title>Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells</title><author>Yao, Zhuocheng ; Zheng, Xianchong ; Lu, Sitong ; He, Zhanxin ; Miao, Yutian ; Huang, Hehai ; Chu, Xinwei ; Cai, Chunqing ; Zou, Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-eefab1387d0c80ccb15d9c732374779e43cc1225afad71ccbce14bae65625e6b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Analysis</topic><topic>Antigens, CD - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cadherins - metabolism</topic><topic>Cancer cells</topic><topic>Cancer Research</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>DNA binding proteins</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>G1 Phase Cell Cycle Checkpoints - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Kaplan-Meier Estimate</topic><topic>MCF-7 Cells</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Prognosis</topic><topic>RNA</topic><topic>RNA Interference</topic><topic>Snail Family Transcription Factors - metabolism</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Transfection</topic><topic>Twist-Related Protein 1 - metabolism</topic><topic>Vimentin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yao, Zhuocheng</creatorcontrib><creatorcontrib>Zheng, Xianchong</creatorcontrib><creatorcontrib>Lu, Sitong</creatorcontrib><creatorcontrib>He, Zhanxin</creatorcontrib><creatorcontrib>Miao, Yutian</creatorcontrib><creatorcontrib>Huang, Hehai</creatorcontrib><creatorcontrib>Chu, Xinwei</creatorcontrib><creatorcontrib>Cai, Chunqing</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><jtitle>Breast cancer (Tokyo, Japan)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yao, Zhuocheng</au><au>Zheng, Xianchong</au><au>Lu, Sitong</au><au>He, Zhanxin</au><au>Miao, Yutian</au><au>Huang, Hehai</au><au>Chu, Xinwei</au><au>Cai, Chunqing</au><au>Zou, Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells</atitle><jtitle>Breast cancer (Tokyo, Japan)</jtitle><stitle>Breast Cancer</stitle><addtitle>Breast Cancer</addtitle><date>2019-11-01</date><risdate>2019</risdate><volume>26</volume><issue>6</issue><spage>835</spage><epage>845</epage><pages>835-845</pages><issn>1340-6868</issn><eissn>1880-4233</eissn><abstract>Background
FAM64A is a mitotic regulator promoting cell metaphase–anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.
Methods
The expression of
FAM64A
mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining. Kaplan–Meier plotter was used to analyze whether FAM64A expression impacted prognosis. Then, the expression of FAM64A was silenced using RNA interference. Cell-counting assay, colony formation assay and flow cytometry assay were conducted to detect proliferation; transwell migration assay, EMT-related proteins expression (E-cadherin, N-cadherin and vimentin), and EMT-related transcription factors mRNA expression (
Snail
,
Twist
,
Slug
) were conducted to evaluate the migration ability.
Results
FAM64A was highly expressed in human BrC samples, which was negatively associated with poor survival time. Analysis of FAM64A expression in BrC cell lines demonstrated that the expression of FAM64A was significantly correlated with the proliferation rate and migration ability of BrC cells. Indeed, knockdown of FAM64A suppressed the proliferation of MDA-MB-231 and MCF-7 cells. Importantly, we also found that silencing of FAM64A inhibited the migration of BrC cells via impeding epithelial–mesenchymal transition.
Conclusions
Our findings suggest that FAM64A plays an important role in the proliferation and migration of BrC cells, which might serve as a potential target for BrC treatment.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>31264076</pmid><doi>10.1007/s12282-019-00991-2</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1340-6868 |
| ispartof | Breast cancer (Tokyo, Japan), 2019-11, Vol.26 (6), p.835-845 |
| issn | 1340-6868 1880-4233 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Analysis Antigens, CD - metabolism Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cadherins - metabolism Cancer cells Cancer Research Cell Movement - genetics Cell Proliferation - genetics DNA binding proteins Epithelial-Mesenchymal Transition - genetics Female G1 Phase Cell Cycle Checkpoints - genetics Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Kaplan-Meier Estimate MCF-7 Cells Medicine Medicine & Public Health Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology Original Article Prognosis RNA RNA Interference Snail Family Transcription Factors - metabolism Surgery Surgical Oncology Transfection Twist-Related Protein 1 - metabolism Vimentin - metabolism |
| title | Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells |
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