Relevance of Abnormal KCNN1 Expression and Osmotic Hypersensitivity in Ewing Sarcoma
Ewing sarcoma (EwS) is a rare and highly malignant bone tumor occurring mainly in childhood and adolescence. Physiologically, the bone is a central hub for Ca homeostasis, which is severely disturbed by osteolytic processes in EwS. Therefore, we aimed to investigate how ion transport proteins involv...
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| Veröffentlicht in: | Cancers 2022-10, Vol.14 (19), p.4819 |
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| creator | Fuest, Sebastian Post, Christoph Balbach, Sebastian T Jabar, Susanne Neumann, Ilka Schimmelpfennig, Sandra Sargin, Sarah Nass, Elke Budde, Thomas Kailayangiri, Sareetha Altvater, Bianca Ranft, Andreas Hartmann, Wolfgang Dirksen, Uta Rössig, Claudia Schwab, Albrecht Pethő, Zoltán |
| description | Ewing sarcoma (EwS) is a rare and highly malignant bone tumor occurring mainly in childhood and adolescence. Physiologically, the bone is a central hub for Ca
homeostasis, which is severely disturbed by osteolytic processes in EwS. Therefore, we aimed to investigate how ion transport proteins involved in Ca
homeostasis affect EwS pathophysiology. We characterized the expression of 22 candidate genes of Ca
-permeable or Ca
-regulated ion channels in three EwS cell lines and found the Ca
-activated K
channel K
2.1 (
) to be exceptionally highly expressed. We revealed that
expression is directly regulated by the disease-driving oncoprotein EWSR1-FL1. Due to its consistent overexpression in EwS,
mRNA could be a prognostic marker in EwS. In a large cohort of EwS patients, however,
mRNA quantity does not correlate with clinical parameters. Several functional studies including patch clamp electrophysiology revealed no evidence for K
2.1 function in EwS cells. Thus, elevated
expression is not translated to K
2.1 channel activity in EwS cells. However, we found that the low K
conductance of EwS cells renders them susceptible to hypoosmotic solutions. The absence of a relevant K
conductance in EwS thereby provides an opportunity for hypoosmotic therapy that can be exploited during tumor surgery. |
| doi_str_mv | 10.3390/cancers14194819 |
| format | Article |
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homeostasis, which is severely disturbed by osteolytic processes in EwS. Therefore, we aimed to investigate how ion transport proteins involved in Ca
homeostasis affect EwS pathophysiology. We characterized the expression of 22 candidate genes of Ca
-permeable or Ca
-regulated ion channels in three EwS cell lines and found the Ca
-activated K
channel K
2.1 (
) to be exceptionally highly expressed. We revealed that
expression is directly regulated by the disease-driving oncoprotein EWSR1-FL1. Due to its consistent overexpression in EwS,
mRNA could be a prognostic marker in EwS. In a large cohort of EwS patients, however,
mRNA quantity does not correlate with clinical parameters. Several functional studies including patch clamp electrophysiology revealed no evidence for K
2.1 function in EwS cells. Thus, elevated
expression is not translated to K
2.1 channel activity in EwS cells. However, we found that the low K
conductance of EwS cells renders them susceptible to hypoosmotic solutions. The absence of a relevant K
conductance in EwS thereby provides an opportunity for hypoosmotic therapy that can be exploited during tumor surgery.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers14194819</identifier><identifier>PMID: 36230742</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Allergic reaction ; Allergy ; Bone tumors ; Calcium channels ; Calcium homeostasis ; Calcium permeability ; Calcium transport ; Channel gating ; Children ; Electrophysiology ; Ewing's sarcoma ; Ewings sarcoma ; FLI-1 protein ; Gene expression ; Generalized linear models ; Genetic aspects ; Health aspects ; Homeostasis ; Hybridization ; Ion channels ; Medical prognosis ; mRNA ; Osmosis ; Osteolysis ; Patients ; Potassium channels (calcium-gated) ; Potassium conductance ; Protein transport ; Software ; Survival analysis</subject><ispartof>Cancers, 2022-10, Vol.14 (19), p.4819</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-d83a57412edc5a9bbc3fd5e3436491c4d374a42d437b4ee25eaca59c6ec185413</citedby><cites>FETCH-LOGICAL-c418t-d83a57412edc5a9bbc3fd5e3436491c4d374a42d437b4ee25eaca59c6ec185413</cites><orcidid>0000-0001-7383-7715 ; 0000-0002-5435-7860 ; 0000-0001-7057-4761 ; 0000-0003-4936-4879 ; 0000-0002-8672-5285 ; 0000-0003-0212-5758</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/PMC9564116/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9564116/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36230742$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fuest, Sebastian</creatorcontrib><creatorcontrib>Post, Christoph</creatorcontrib><creatorcontrib>Balbach, Sebastian T</creatorcontrib><creatorcontrib>Jabar, Susanne</creatorcontrib><creatorcontrib>Neumann, Ilka</creatorcontrib><creatorcontrib>Schimmelpfennig, Sandra</creatorcontrib><creatorcontrib>Sargin, Sarah</creatorcontrib><creatorcontrib>Nass, Elke</creatorcontrib><creatorcontrib>Budde, Thomas</creatorcontrib><creatorcontrib>Kailayangiri, Sareetha</creatorcontrib><creatorcontrib>Altvater, Bianca</creatorcontrib><creatorcontrib>Ranft, Andreas</creatorcontrib><creatorcontrib>Hartmann, Wolfgang</creatorcontrib><creatorcontrib>Dirksen, Uta</creatorcontrib><creatorcontrib>Rössig, Claudia</creatorcontrib><creatorcontrib>Schwab, Albrecht</creatorcontrib><creatorcontrib>Pethő, Zoltán</creatorcontrib><title>Relevance of Abnormal KCNN1 Expression and Osmotic Hypersensitivity in Ewing Sarcoma</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Ewing sarcoma (EwS) is a rare and highly malignant bone tumor occurring mainly in childhood and adolescence. Physiologically, the bone is a central hub for Ca
homeostasis, which is severely disturbed by osteolytic processes in EwS. Therefore, we aimed to investigate how ion transport proteins involved in Ca
homeostasis affect EwS pathophysiology. We characterized the expression of 22 candidate genes of Ca
-permeable or Ca
-regulated ion channels in three EwS cell lines and found the Ca
-activated K
channel K
2.1 (
) to be exceptionally highly expressed. We revealed that
expression is directly regulated by the disease-driving oncoprotein EWSR1-FL1. Due to its consistent overexpression in EwS,
mRNA could be a prognostic marker in EwS. In a large cohort of EwS patients, however,
mRNA quantity does not correlate with clinical parameters. Several functional studies including patch clamp electrophysiology revealed no evidence for K
2.1 function in EwS cells. Thus, elevated
expression is not translated to K
2.1 channel activity in EwS cells. However, we found that the low K
conductance of EwS cells renders them susceptible to hypoosmotic solutions. The absence of a relevant K
conductance in EwS thereby provides an opportunity for hypoosmotic therapy that can be exploited during tumor surgery.</description><subject>Allergic reaction</subject><subject>Allergy</subject><subject>Bone tumors</subject><subject>Calcium channels</subject><subject>Calcium homeostasis</subject><subject>Calcium permeability</subject><subject>Calcium transport</subject><subject>Channel gating</subject><subject>Children</subject><subject>Electrophysiology</subject><subject>Ewing's sarcoma</subject><subject>Ewings sarcoma</subject><subject>FLI-1 protein</subject><subject>Gene expression</subject><subject>Generalized linear models</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Hybridization</subject><subject>Ion channels</subject><subject>Medical prognosis</subject><subject>mRNA</subject><subject>Osmosis</subject><subject>Osteolysis</subject><subject>Patients</subject><subject>Potassium channels (calcium-gated)</subject><subject>Potassium conductance</subject><subject>Protein transport</subject><subject>Software</subject><subject>Survival 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Sebastian</creator><creator>Post, Christoph</creator><creator>Balbach, Sebastian T</creator><creator>Jabar, Susanne</creator><creator>Neumann, Ilka</creator><creator>Schimmelpfennig, Sandra</creator><creator>Sargin, Sarah</creator><creator>Nass, Elke</creator><creator>Budde, Thomas</creator><creator>Kailayangiri, Sareetha</creator><creator>Altvater, Bianca</creator><creator>Ranft, Andreas</creator><creator>Hartmann, Wolfgang</creator><creator>Dirksen, Uta</creator><creator>Rössig, Claudia</creator><creator>Schwab, Albrecht</creator><creator>Pethő, Zoltán</creator><general>MDPI 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of Abnormal KCNN1 Expression and Osmotic Hypersensitivity in Ewing Sarcoma</title><author>Fuest, Sebastian ; Post, Christoph ; Balbach, Sebastian T ; Jabar, Susanne ; Neumann, Ilka ; Schimmelpfennig, Sandra ; Sargin, Sarah ; Nass, Elke ; Budde, Thomas ; Kailayangiri, Sareetha ; Altvater, Bianca ; Ranft, Andreas ; Hartmann, Wolfgang ; Dirksen, Uta ; Rössig, Claudia ; Schwab, Albrecht ; Pethő, Zoltán</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-d83a57412edc5a9bbc3fd5e3436491c4d374a42d437b4ee25eaca59c6ec185413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Allergic reaction</topic><topic>Allergy</topic><topic>Bone tumors</topic><topic>Calcium channels</topic><topic>Calcium homeostasis</topic><topic>Calcium permeability</topic><topic>Calcium transport</topic><topic>Channel gating</topic><topic>Children</topic><topic>Electrophysiology</topic><topic>Ewing's sarcoma</topic><topic>Ewings sarcoma</topic><topic>FLI-1 protein</topic><topic>Gene expression</topic><topic>Generalized linear models</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Hybridization</topic><topic>Ion channels</topic><topic>Medical prognosis</topic><topic>mRNA</topic><topic>Osmosis</topic><topic>Osteolysis</topic><topic>Patients</topic><topic>Potassium channels (calcium-gated)</topic><topic>Potassium conductance</topic><topic>Protein transport</topic><topic>Software</topic><topic>Survival analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fuest, Sebastian</creatorcontrib><creatorcontrib>Post, Christoph</creatorcontrib><creatorcontrib>Balbach, Sebastian T</creatorcontrib><creatorcontrib>Jabar, Susanne</creatorcontrib><creatorcontrib>Neumann, Ilka</creatorcontrib><creatorcontrib>Schimmelpfennig, Sandra</creatorcontrib><creatorcontrib>Sargin, Sarah</creatorcontrib><creatorcontrib>Nass, Elke</creatorcontrib><creatorcontrib>Budde, Thomas</creatorcontrib><creatorcontrib>Kailayangiri, Sareetha</creatorcontrib><creatorcontrib>Altvater, Bianca</creatorcontrib><creatorcontrib>Ranft, Andreas</creatorcontrib><creatorcontrib>Hartmann, Wolfgang</creatorcontrib><creatorcontrib>Dirksen, Uta</creatorcontrib><creatorcontrib>Rössig, Claudia</creatorcontrib><creatorcontrib>Schwab, Albrecht</creatorcontrib><creatorcontrib>Pethő, Zoltán</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 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Abnormal KCNN1 Expression and Osmotic Hypersensitivity in Ewing Sarcoma</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2022-10-01</date><risdate>2022</risdate><volume>14</volume><issue>19</issue><spage>4819</spage><pages>4819-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Ewing sarcoma (EwS) is a rare and highly malignant bone tumor occurring mainly in childhood and adolescence. Physiologically, the bone is a central hub for Ca
homeostasis, which is severely disturbed by osteolytic processes in EwS. Therefore, we aimed to investigate how ion transport proteins involved in Ca
homeostasis affect EwS pathophysiology. We characterized the expression of 22 candidate genes of Ca
-permeable or Ca
-regulated ion channels in three EwS cell lines and found the Ca
-activated K
channel K
2.1 (
) to be exceptionally highly expressed. We revealed that
expression is directly regulated by the disease-driving oncoprotein EWSR1-FL1. Due to its consistent overexpression in EwS,
mRNA could be a prognostic marker in EwS. In a large cohort of EwS patients, however,
mRNA quantity does not correlate with clinical parameters. Several functional studies including patch clamp electrophysiology revealed no evidence for K
2.1 function in EwS cells. Thus, elevated
expression is not translated to K
2.1 channel activity in EwS cells. However, we found that the low K
conductance of EwS cells renders them susceptible to hypoosmotic solutions. The absence of a relevant K
conductance in EwS thereby provides an opportunity for hypoosmotic therapy that can be exploited during tumor surgery.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36230742</pmid><doi>10.3390/cancers14194819</doi><orcidid>https://orcid.org/0000-0001-7383-7715</orcidid><orcidid>https://orcid.org/0000-0002-5435-7860</orcidid><orcidid>https://orcid.org/0000-0001-7057-4761</orcidid><orcidid>https://orcid.org/0000-0003-4936-4879</orcidid><orcidid>https://orcid.org/0000-0002-8672-5285</orcidid><orcidid>https://orcid.org/0000-0003-0212-5758</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancers, 2022-10, Vol.14 (19), p.4819 |
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| source | PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Allergic reaction Allergy Bone tumors Calcium channels Calcium homeostasis Calcium permeability Calcium transport Channel gating Children Electrophysiology Ewing's sarcoma Ewings sarcoma FLI-1 protein Gene expression Generalized linear models Genetic aspects Health aspects Homeostasis Hybridization Ion channels Medical prognosis mRNA Osmosis Osteolysis Patients Potassium channels (calcium-gated) Potassium conductance Protein transport Software Survival analysis |
| title | Relevance of Abnormal KCNN1 Expression and Osmotic Hypersensitivity in Ewing Sarcoma |
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