Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms
Advanced prostate cancers that progress to tumor metastases are often considered incurable or difficult to treat. The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated w...
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| Veröffentlicht in: | Cancers 2020-04, Vol.12 (5), p.1071 |
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| description | Advanced prostate cancers that progress to tumor metastases are often considered incurable or difficult to treat. The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated with tumor progression. Calcium plays a relevant role on tumor cell death, proliferation, motility-invasion and tumor metastasis. Calcium controls molecular factors and signaling pathways involved in the development of prostate cancer and its progression. Such factors and pathways include calcium channels and calcium-binding proteins. Nevertheless, the involvement of calcium signaling on prostate cancer predisposition for bone tropism has been relatively unexplored. In this regard, a diversity of mechanisms triggers transient accumulation of intracellular calcium in prostate cancer cells, potentially favoring bone metastases development. New therapies for the treatment of prostate cancer include compounds characterized by potent and specific actions that target calcium channels/transporters or pumps. These novel drugs for prostate cancer treatment encompass calcium-ATPase inhibitors, voltage-gated calcium channel inhibitors, transient receptor potential (TRP) channel regulators or Orai inhibitors. This review details the latest results that have evaluated the relationship between calcium signaling and progression of prostate cancer, as well as potential therapies aiming to modulate calcium signaling in prostate tumor progression. |
| doi_str_mv | 10.3390/cancers12051071 |
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The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated with tumor progression. Calcium plays a relevant role on tumor cell death, proliferation, motility-invasion and tumor metastasis. Calcium controls molecular factors and signaling pathways involved in the development of prostate cancer and its progression. Such factors and pathways include calcium channels and calcium-binding proteins. Nevertheless, the involvement of calcium signaling on prostate cancer predisposition for bone tropism has been relatively unexplored. In this regard, a diversity of mechanisms triggers transient accumulation of intracellular calcium in prostate cancer cells, potentially favoring bone metastases development. New therapies for the treatment of prostate cancer include compounds characterized by potent and specific actions that target calcium channels/transporters or pumps. These novel drugs for prostate cancer treatment encompass calcium-ATPase inhibitors, voltage-gated calcium channel inhibitors, transient receptor potential (TRP) channel regulators or Orai inhibitors. This review details the latest results that have evaluated the relationship between calcium signaling and progression of prostate cancer, as well as potential therapies aiming to modulate calcium signaling in prostate tumor progression.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers12051071</identifier><identifier>PMID: 32344908</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Androgens ; Apoptosis ; Bone cancer ; Ca2+-transporting ATPase ; Calcium (intracellular) ; Calcium channels ; Calcium channels (voltage-gated) ; Calcium signalling ; Cancer therapies ; Cell adhesion & migration ; Cell death ; Cell growth ; Endoplasmic reticulum ; Etiology ; Gene expression ; Homeostasis ; Localization ; Medical prognosis ; Metastases ; Metastasis ; Mitochondria ; Mortality ; Prostate cancer ; Proteins ; Review ; Signal transduction ; Transient receptor potential proteins ; Tropism ; Tumor cells ; Tumors</subject><ispartof>Cancers, 2020-04, Vol.12 (5), p.1071</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-798a4e940eab68b74e699af281691c1e3e13d564086500e0818a9a9bc2c050ad3</citedby><cites>FETCH-LOGICAL-c487t-798a4e940eab68b74e699af281691c1e3e13d564086500e0818a9a9bc2c050ad3</cites><orcidid>0000-0002-2813-3257 ; 0000-0002-2827-3364 ; 0000-0001-9686-672X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7281772/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7281772/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32344908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ardura, Juan A</creatorcontrib><creatorcontrib>Álvarez-Carrión, Luis</creatorcontrib><creatorcontrib>Gutiérrez-Rojas, Irene</creatorcontrib><creatorcontrib>Alonso, Verónica</creatorcontrib><title>Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Advanced prostate cancers that progress to tumor metastases are often considered incurable or difficult to treat. The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated with tumor progression. Calcium plays a relevant role on tumor cell death, proliferation, motility-invasion and tumor metastasis. Calcium controls molecular factors and signaling pathways involved in the development of prostate cancer and its progression. Such factors and pathways include calcium channels and calcium-binding proteins. Nevertheless, the involvement of calcium signaling on prostate cancer predisposition for bone tropism has been relatively unexplored. In this regard, a diversity of mechanisms triggers transient accumulation of intracellular calcium in prostate cancer cells, potentially favoring bone metastases development. New therapies for the treatment of prostate cancer include compounds characterized by potent and specific actions that target calcium channels/transporters or pumps. These novel drugs for prostate cancer treatment encompass calcium-ATPase inhibitors, voltage-gated calcium channel inhibitors, transient receptor potential (TRP) channel regulators or Orai inhibitors. This review details the latest results that have evaluated the relationship between calcium signaling and progression of prostate cancer, as well as potential therapies aiming to modulate calcium signaling in prostate tumor progression.</description><subject>Androgens</subject><subject>Apoptosis</subject><subject>Bone cancer</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium (intracellular)</subject><subject>Calcium channels</subject><subject>Calcium channels (voltage-gated)</subject><subject>Calcium signalling</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Endoplasmic reticulum</subject><subject>Etiology</subject><subject>Gene expression</subject><subject>Homeostasis</subject><subject>Localization</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Mortality</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Review</subject><subject>Signal transduction</subject><subject>Transient receptor potential proteins</subject><subject>Tropism</subject><subject>Tumor cells</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdUctuFDEQtBCIRCFnbsgSFy6b2GOPHxyQYJUQpCAQj7PV6-3ZOHjsYM8g8fd4tEkU4ou7VeXqdhUhLzk7EcKyUw_JY6m8Yz1nmj8hhx3T3UopK58-qA_Ica3XrB0huFb6OTkQnZDSMnNIpm85Is0DXUP0YR7p97BLEEPa0ZDo15LrBBM2dBm19LuCtYac3tKzYUA_VZrTHXwBMY5QflUKaUs_5IT0M06wSATfSn8FKdSxviDPBogVj2_vI_Lz_OzH-mJ1-eXjp_X7y5WXRk8rbQ1ItJIhbJTZaInKWhg6w5XlnqNALra9ksyonjFkhhuwYDe-86xnsBVH5N1e92bejLj1mKYC0d2U0Lb86zIE9z-SwpXb5T9Otxlad03gza1Ayb9nrJMbQ_UYIyTMc3WdsEo09_uF-voR9TrPpVm5Z_Wqk0Y01ume5ZuzteBwvwxnbgnVPQq1vXj18A_3_LsIxT9cZZ7n</recordid><startdate>20200425</startdate><enddate>20200425</enddate><creator>Ardura, Juan A</creator><creator>Álvarez-Carrión, Luis</creator><creator>Gutiérrez-Rojas, Irene</creator><creator>Alonso, Verónica</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2813-3257</orcidid><orcidid>https://orcid.org/0000-0002-2827-3364</orcidid><orcidid>https://orcid.org/0000-0001-9686-672X</orcidid></search><sort><creationdate>20200425</creationdate><title>Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms</title><author>Ardura, Juan A ; Álvarez-Carrión, Luis ; Gutiérrez-Rojas, Irene ; Alonso, Verónica</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-798a4e940eab68b74e699af281691c1e3e13d564086500e0818a9a9bc2c050ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Androgens</topic><topic>Apoptosis</topic><topic>Bone cancer</topic><topic>Ca2+-transporting ATPase</topic><topic>Calcium (intracellular)</topic><topic>Calcium channels</topic><topic>Calcium channels (voltage-gated)</topic><topic>Calcium signalling</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Endoplasmic reticulum</topic><topic>Etiology</topic><topic>Gene expression</topic><topic>Homeostasis</topic><topic>Localization</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mitochondria</topic><topic>Mortality</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Review</topic><topic>Signal transduction</topic><topic>Transient receptor potential proteins</topic><topic>Tropism</topic><topic>Tumor cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ardura, Juan A</creatorcontrib><creatorcontrib>Álvarez-Carrión, Luis</creatorcontrib><creatorcontrib>Gutiérrez-Rojas, Irene</creatorcontrib><creatorcontrib>Alonso, Verónica</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ardura, Juan A</au><au>Álvarez-Carrión, Luis</au><au>Gutiérrez-Rojas, Irene</au><au>Alonso, Verónica</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2020-04-25</date><risdate>2020</risdate><volume>12</volume><issue>5</issue><spage>1071</spage><pages>1071-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Advanced prostate cancers that progress to tumor metastases are often considered incurable or difficult to treat. The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated with tumor progression. Calcium plays a relevant role on tumor cell death, proliferation, motility-invasion and tumor metastasis. Calcium controls molecular factors and signaling pathways involved in the development of prostate cancer and its progression. Such factors and pathways include calcium channels and calcium-binding proteins. Nevertheless, the involvement of calcium signaling on prostate cancer predisposition for bone tropism has been relatively unexplored. In this regard, a diversity of mechanisms triggers transient accumulation of intracellular calcium in prostate cancer cells, potentially favoring bone metastases development. New therapies for the treatment of prostate cancer include compounds characterized by potent and specific actions that target calcium channels/transporters or pumps. These novel drugs for prostate cancer treatment encompass calcium-ATPase inhibitors, voltage-gated calcium channel inhibitors, transient receptor potential (TRP) channel regulators or Orai inhibitors. This review details the latest results that have evaluated the relationship between calcium signaling and progression of prostate cancer, as well as potential therapies aiming to modulate calcium signaling in prostate tumor progression.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32344908</pmid><doi>10.3390/cancers12051071</doi><orcidid>https://orcid.org/0000-0002-2813-3257</orcidid><orcidid>https://orcid.org/0000-0002-2827-3364</orcidid><orcidid>https://orcid.org/0000-0001-9686-672X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Androgens Apoptosis Bone cancer Ca2+-transporting ATPase Calcium (intracellular) Calcium channels Calcium channels (voltage-gated) Calcium signalling Cancer therapies Cell adhesion & migration Cell death Cell growth Endoplasmic reticulum Etiology Gene expression Homeostasis Localization Medical prognosis Metastases Metastasis Mitochondria Mortality Prostate cancer Proteins Review Signal transduction Transient receptor potential proteins Tropism Tumor cells Tumors |
| title | Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms |
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