SMARCAD1 in Breast Cancer Progression
Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-ca...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2018-10, Vol.50 (2), p.489-500 |
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| creator | Arafat, Kholoud Al Kubaisy, Elham Sulaiman, Shahrazad Karam, Sherif M. Al Natour, Zeina Hassan, Ahmed H. Attoub, Samir |
| description | Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER - /PR - / HER2 - ) and T47D (ER + /PR +/- /HER2 - ) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy. |
| doi_str_mv | 10.1159/000494163 |
| format | Article |
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The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER - /PR - / HER2 - ) and T47D (ER + /PR +/- /HER2 - ) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000494163</identifier><identifier>PMID: 30308496</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Binding sites ; Bladder cancer ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell adhesion & migration ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chick Embryo ; Deoxyribonucleic acid ; Development and progression ; Disease Progression ; DNA ; DNA Helicases - antagonists & inhibitors ; DNA Helicases - genetics ; DNA Helicases - metabolism ; Female ; Gene expression ; Genetic aspects ; Health aspects ; Helicases ; Humans ; I-kappa B Kinase - antagonists & inhibitors ; I-kappa B Kinase - genetics ; I-kappa B Kinase - metabolism ; IKK ; Kinases ; Metastasis ; Mice ; Mice, Nude ; Original Paper ; Phosphorylation ; Physiological aspects ; RNA Interference ; RNA, Small Interfering - metabolism ; SMARCAD1 ; Tumor growth ; Xenograft Model Antitumor Assays</subject><ispartof>Cellular Physiology and Biochemistry, 2018-10, Vol.50 (2), p.489-500</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2018 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-4e2c4e57d06304bcb47446e793937826b039ac1aaf3d639056b132e0e3970963</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30308496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arafat, Kholoud</creatorcontrib><creatorcontrib>Al Kubaisy, Elham</creatorcontrib><creatorcontrib>Sulaiman, Shahrazad</creatorcontrib><creatorcontrib>Karam, Sherif M.</creatorcontrib><creatorcontrib>Al Natour, Zeina</creatorcontrib><creatorcontrib>Hassan, Ahmed H.</creatorcontrib><creatorcontrib>Attoub, Samir </creatorcontrib><title>SMARCAD1 in Breast Cancer Progression</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER - /PR - / HER2 - ) and T47D (ER + /PR +/- /HER2 - ) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.</description><subject>Animals</subject><subject>Binding sites</subject><subject>Bladder cancer</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Chick Embryo</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>DNA</subject><subject>DNA Helicases - antagonists & inhibitors</subject><subject>DNA Helicases - genetics</subject><subject>DNA Helicases - metabolism</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Helicases</subject><subject>Humans</subject><subject>I-kappa B Kinase - antagonists & inhibitors</subject><subject>I-kappa B Kinase - genetics</subject><subject>I-kappa B Kinase - metabolism</subject><subject>IKK</subject><subject>Kinases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Original Paper</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>SMARCAD1</subject><subject>Tumor growth</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNpdkUFvFDEMhUcIREvhwB2hlRASPUyx40wyOS4LlEpFIOg9ymQ8qyy7k5LMHvrvSTvLHiofYlufn2O9qnqNcIHYmI8AII1ERU-qU5QCa6N1-7TkgE3dmlafVC9y3kAptRHPqxMCglYadVq9__19-Wu1_IyLMC4-JXZ5Wqzc6Dktfqa4TpxziOPL6tngtplfHd6z6ubrl5vVt_r6x-XVanld-wbEVEsWXnKje1AEsvOd1FIq1oYM6VaoDsg4j84N1Csy0KgOSTAwGQ1G0Vl1Ncv20W3sbQo7l-5sdME-NGJaW5em4Ldse9Vr16FqWqEl49A1gxGOSXReKoeiaH2YtW5T_LvnPNldyJ63Wzdy3GcrEI0h0HC_9t0jdBP3aSyHWkGArZEadKEuZmrtyv4wDnFKzpfoeRd8HHkIpb9UpBtCepA9nwd8ijknHo4XIdh73-zRt8K-PXxh3-24P5L_jSrAmxn449Ka0xE4zP8DyCqVLw</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Arafat, Kholoud</creator><creator>Al Kubaisy, Elham</creator><creator>Sulaiman, Shahrazad</creator><creator>Karam, Sherif M.</creator><creator>Al Natour, Zeina</creator><creator>Hassan, Ahmed H.</creator><creator>Attoub, Samir </creator><general>S. 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metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Chick Embryo</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>Disease Progression</topic><topic>DNA</topic><topic>DNA Helicases - antagonists & inhibitors</topic><topic>DNA Helicases - genetics</topic><topic>DNA Helicases - metabolism</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Helicases</topic><topic>Humans</topic><topic>I-kappa B Kinase - antagonists & inhibitors</topic><topic>I-kappa B Kinase - genetics</topic><topic>I-kappa B Kinase - metabolism</topic><topic>IKK</topic><topic>Kinases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Original Paper</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>SMARCAD1</topic><topic>Tumor growth</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arafat, Kholoud</creatorcontrib><creatorcontrib>Al Kubaisy, Elham</creatorcontrib><creatorcontrib>Sulaiman, Shahrazad</creatorcontrib><creatorcontrib>Karam, Sherif M.</creatorcontrib><creatorcontrib>Al Natour, Zeina</creatorcontrib><creatorcontrib>Hassan, Ahmed H.</creatorcontrib><creatorcontrib>Attoub, Samir </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>MEDLINE - Academic</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>Arafat, Kholoud</au><au>Al Kubaisy, Elham</au><au>Sulaiman, Shahrazad</au><au>Karam, Sherif M.</au><au>Al Natour, Zeina</au><au>Hassan, Ahmed H.</au><au>Attoub, Samir </au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SMARCAD1 in Breast Cancer Progression</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>50</volume><issue>2</issue><spage>489</spage><epage>500</epage><pages>489-500</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER - /PR - / HER2 - ) and T47D (ER + /PR +/- /HER2 - ) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30308496</pmid><doi>10.1159/000494163</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Binding sites Bladder cancer Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell adhesion & migration Cell cycle Cell growth Cell Line, Tumor Cell Movement Cell Proliferation Chick Embryo Deoxyribonucleic acid Development and progression Disease Progression DNA DNA Helicases - antagonists & inhibitors DNA Helicases - genetics DNA Helicases - metabolism Female Gene expression Genetic aspects Health aspects Helicases Humans I-kappa B Kinase - antagonists & inhibitors I-kappa B Kinase - genetics I-kappa B Kinase - metabolism IKK Kinases Metastasis Mice Mice, Nude Original Paper Phosphorylation Physiological aspects RNA Interference RNA, Small Interfering - metabolism SMARCAD1 Tumor growth Xenograft Model Antitumor Assays |
| title | SMARCAD1 in Breast Cancer Progression |
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