CdGAP promotes prostate cancer metastasis by regulating epithelial-to-mesenchymal transition, cell cycle progression, and apoptosis
High mortality of prostate cancer patients is primarily due to metastasis. Understanding the mechanisms controlling metastatic processes remains essential to develop novel therapies designed to prevent the progression from localized disease to metastasis. CdGAP plays important roles in the control o...
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| Veröffentlicht in: | Communications biology 2021-09, Vol.4 (1), p.1042-1042, Article 1042 |
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| creator | Mehra, Chahat Chung, Ji-Hyun He, Yi Lara-Márquez, Mónica Goyette, Marie-Anne Boufaied, Nadia Barrès, Véronique Ouellet, Véronique Guérard, Karl-Phillippe Delliaux, Carine Saad, Fred Lapointe, Jacques Côté, Jean-François Labbé, David P. Lamarche-Vane, Nathalie |
| description | High mortality of prostate cancer patients is primarily due to metastasis. Understanding the mechanisms controlling metastatic processes remains essential to develop novel therapies designed to prevent the progression from localized disease to metastasis. CdGAP plays important roles in the control of cell adhesion, migration, and proliferation, which are central to cancer progression. Here we show that elevated CdGAP expression is associated with early biochemical recurrence and bone metastasis in prostate cancer patients. Knockdown of CdGAP in metastatic castration-resistant prostate cancer (CRPC) PC-3 and 22Rv1 cells reduces cell motility, invasion, and proliferation while inducing apoptosis in CdGAP-depleted PC-3 cells. Conversely, overexpression of CdGAP in DU-145, 22Rv1, and LNCaP cells increases cell migration and invasion. Using global gene expression approaches, we found that CdGAP regulates the expression of genes involved in epithelial-to-mesenchymal transition, apoptosis and cell cycle progression. Subcutaneous injection of CdGAP-depleted PC-3 cells into mice shows a delayed tumor initiation and attenuated tumor growth. Orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastasic burden. Collectively, these findings support a pro-oncogenic role of CdGAP in prostate tumorigenesis and unveil CdGAP as a potential biomarker and target for prostate cancer treatments.
Mehra et al. investigate the role of CdGAP in early biochemical recurrence and bone metastasis in prostate cancer. The authors find that knocking down CdGAP leads to reduced cell motility, invasion and proliferation in PC-3 and 22Rv1 cells while orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastatic burden. |
| doi_str_mv | 10.1038/s42003-021-02520-4 |
| format | Article |
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Mehra et al. investigate the role of CdGAP in early biochemical recurrence and bone metastasis in prostate cancer. The authors find that knocking down CdGAP leads to reduced cell motility, invasion and proliferation in PC-3 and 22Rv1 cells while orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastatic burden.</description><identifier>ISSN: 2399-3642</identifier><identifier>EISSN: 2399-3642</identifier><identifier>DOI: 10.1038/s42003-021-02520-4</identifier><identifier>PMID: 34493786</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/1 ; 13/105 ; 13/106 ; 13/109 ; 13/2 ; 13/31 ; 13/51 ; 13/95 ; 14 ; 14/19 ; 45 ; 45/91 ; 631/67/322/803 ; 631/67/589 ; 64 ; 692/4028/67/322 ; Animals ; Apoptosis ; Biology ; Biomedical and Life Sciences ; Bone cancer ; Castration ; Cell adhesion ; Cell Cycle ; Cell migration ; Cell proliferation ; Epithelial-Mesenchymal Transition ; Gene expression ; Injection ; Life Sciences ; Life Sciences & Biomedicine ; Life Sciences & Biomedicine - Other Topics ; Male ; Mesenchyme ; Metastases ; Metastasis ; Mice ; Mice, Nude ; Motility ; Multidisciplinary Sciences ; Neoplasm Metastasis ; Prostate cancer ; Prostatic Neoplasms - pathology ; Science & Technology ; Science & Technology - Other Topics ; Tumorigenesis</subject><ispartof>Communications biology, 2021-09, Vol.4 (1), p.1042-1042, Article 1042</ispartof><rights>The Author(s) 2021</rights><rights>2021. The Author(s).</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Understanding the mechanisms controlling metastatic processes remains essential to develop novel therapies designed to prevent the progression from localized disease to metastasis. CdGAP plays important roles in the control of cell adhesion, migration, and proliferation, which are central to cancer progression. Here we show that elevated CdGAP expression is associated with early biochemical recurrence and bone metastasis in prostate cancer patients. Knockdown of CdGAP in metastatic castration-resistant prostate cancer (CRPC) PC-3 and 22Rv1 cells reduces cell motility, invasion, and proliferation while inducing apoptosis in CdGAP-depleted PC-3 cells. Conversely, overexpression of CdGAP in DU-145, 22Rv1, and LNCaP cells increases cell migration and invasion. Using global gene expression approaches, we found that CdGAP regulates the expression of genes involved in epithelial-to-mesenchymal transition, apoptosis and cell cycle progression. Subcutaneous injection of CdGAP-depleted PC-3 cells into mice shows a delayed tumor initiation and attenuated tumor growth. Orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastasic burden. Collectively, these findings support a pro-oncogenic role of CdGAP in prostate tumorigenesis and unveil CdGAP as a potential biomarker and target for prostate cancer treatments.
Mehra et al. investigate the role of CdGAP in early biochemical recurrence and bone metastasis in prostate cancer. The authors find that knocking down CdGAP leads to reduced cell motility, invasion and proliferation in PC-3 and 22Rv1 cells while orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastatic burden.</description><subject>13</subject><subject>13/1</subject><subject>13/105</subject><subject>13/106</subject><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>13/51</subject><subject>13/95</subject><subject>14</subject><subject>14/19</subject><subject>45</subject><subject>45/91</subject><subject>631/67/322/803</subject><subject>631/67/589</subject><subject>64</subject><subject>692/4028/67/322</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biology</subject><subject>Biomedical and Life Sciences</subject><subject>Bone cancer</subject><subject>Castration</subject><subject>Cell adhesion</subject><subject>Cell Cycle</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Epithelial-Mesenchymal 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Nathalie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CdGAP promotes prostate cancer metastasis by regulating epithelial-to-mesenchymal transition, cell cycle progression, and apoptosis</atitle><jtitle>Communications biology</jtitle><stitle>Commun Biol</stitle><stitle>COMMUN BIOL</stitle><addtitle>Commun Biol</addtitle><date>2021-09-07</date><risdate>2021</risdate><volume>4</volume><issue>1</issue><spage>1042</spage><epage>1042</epage><pages>1042-1042</pages><artnum>1042</artnum><issn>2399-3642</issn><eissn>2399-3642</eissn><abstract>High mortality of prostate cancer patients is primarily due to metastasis. Understanding the mechanisms controlling metastatic processes remains essential to develop novel therapies designed to prevent the progression from localized disease to metastasis. CdGAP plays important roles in the control of cell adhesion, migration, and proliferation, which are central to cancer progression. Here we show that elevated CdGAP expression is associated with early biochemical recurrence and bone metastasis in prostate cancer patients. Knockdown of CdGAP in metastatic castration-resistant prostate cancer (CRPC) PC-3 and 22Rv1 cells reduces cell motility, invasion, and proliferation while inducing apoptosis in CdGAP-depleted PC-3 cells. Conversely, overexpression of CdGAP in DU-145, 22Rv1, and LNCaP cells increases cell migration and invasion. Using global gene expression approaches, we found that CdGAP regulates the expression of genes involved in epithelial-to-mesenchymal transition, apoptosis and cell cycle progression. Subcutaneous injection of CdGAP-depleted PC-3 cells into mice shows a delayed tumor initiation and attenuated tumor growth. Orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastasic burden. Collectively, these findings support a pro-oncogenic role of CdGAP in prostate tumorigenesis and unveil CdGAP as a potential biomarker and target for prostate cancer treatments.
Mehra et al. investigate the role of CdGAP in early biochemical recurrence and bone metastasis in prostate cancer. The authors find that knocking down CdGAP leads to reduced cell motility, invasion and proliferation in PC-3 and 22Rv1 cells while orthotopic injection of CdGAP-depleted PC-3 cells reduces distant metastatic burden.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>34493786</pmid><doi>10.1038/s42003-021-02520-4</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-1854-7082</orcidid><orcidid>https://orcid.org/0000-0003-3199-2252</orcidid><orcidid>https://orcid.org/0000-0001-8864-8765</orcidid><orcidid>https://orcid.org/0000-0002-9540-3157</orcidid><orcidid>https://orcid.org/0000-0001-7055-2642</orcidid><orcidid>https://orcid.org/0000-0002-4586-8052</orcidid><orcidid>https://orcid.org/0000-0003-3338-1527</orcidid><orcidid>https://orcid.org/0000-0002-7229-3952</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 2399-3642 |
| ispartof | Communications biology, 2021-09, Vol.4 (1), p.1042-1042, Article 1042 |
| issn | 2399-3642 2399-3642 |
| language | eng |
| recordid | cdi_pubmed_primary_34493786 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Nature Free; Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; PubMed Central; Springer Nature OA/Free Journals |
| subjects | 13 13/1 13/105 13/106 13/109 13/2 13/31 13/51 13/95 14 14/19 45 45/91 631/67/322/803 631/67/589 64 692/4028/67/322 Animals Apoptosis Biology Biomedical and Life Sciences Bone cancer Castration Cell adhesion Cell Cycle Cell migration Cell proliferation Epithelial-Mesenchymal Transition Gene expression Injection Life Sciences Life Sciences & Biomedicine Life Sciences & Biomedicine - Other Topics Male Mesenchyme Metastases Metastasis Mice Mice, Nude Motility Multidisciplinary Sciences Neoplasm Metastasis Prostate cancer Prostatic Neoplasms - pathology Science & Technology Science & Technology - Other Topics Tumorigenesis |
| title | CdGAP promotes prostate cancer metastasis by regulating epithelial-to-mesenchymal transition, cell cycle progression, and apoptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-12T02%3A21%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CdGAP%20promotes%20prostate%20cancer%20metastasis%20by%20regulating%20epithelial-to-mesenchymal%20transition,%20cell%20cycle%20progression,%20and%20apoptosis&rft.jtitle=Communications%20biology&rft.au=Mehra,%20Chahat&rft.date=2021-09-07&rft.volume=4&rft.issue=1&rft.spage=1042&rft.epage=1042&rft.pages=1042-1042&rft.artnum=1042&rft.issn=2399-3642&rft.eissn=2399-3642&rft_id=info:doi/10.1038/s42003-021-02520-4&rft_dat=%3Cproquest_pubme%3E2569856227%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2569856227&rft_id=info:pmid/34493786&rft_doaj_id=oai_doaj_org_article_90e48f7b139747d6ba6e98b737476318&rfr_iscdi=true |