Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways
The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell prolife...
Gespeichert in:
| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2023-08, Vol.80 (8), p.202-202, Article 202 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 202 |
|---|---|
| container_issue | 8 |
| container_start_page | 202 |
| container_title | Cellular and molecular life sciences : CMLS |
| container_volume | 80 |
| creator | Tito, Claudia Genovese, Ilaria Giamogante, Flavia Benedetti, Anna Miglietta, Selenia Barazzuol, Lucia Cristiano, Loredana Iaiza, Alessia Carolini, Sabatino De Angelis, Luciana Masciarelli, Silvia Nottola, Stefania Annarita Familiari, Giuseppe Petrozza, Vincenzo Lauriola, Mattia Tamagnone, Luca Ilari, Andrea Calì, Tito Valdivia, Hector H. Valdivia, Carmen R. Colotti, Gianni Fazi, Francesco |
| description | The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies. |
| doi_str_mv | 10.1007/s00018-023-04850-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10345051</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3040424906</sourcerecordid><originalsourceid>FETCH-LOGICAL-c508t-9f9bd2b5a7978e9294cc10b0572aa9548a2ad126a56081d62ff19427236b55c53</originalsourceid><addsrcrecordid>eNqFkUtrFTEYhoMotlb_gAsZcONm9Mt1kpVI6Q0KQlUQXIRMJjMnZSYZk5lK_705Pcd6WdhVLt-TN1_yIPQSw1sM0LzLAIBlDYTWwCSHmj1Ch5gRqBU0-PF-LiT5eoCe5XxdaC6JeIoOaMMYkUQeom-fYrI-VHOKU1xcriY_JLP4GKqya02wLlUmdFVywzqaLbFsXHVydlp3bnahc2HZrq6q7IdgRh-GajbL5oe5zc_Rk96M2b3Yj0foy-nJ5-Pz-vLj2cXxh8vacpBLrXrVdqTlplGNdIooZi2GFnhDjFGcSUNMh4kwXIDEnSB9jxUjDaGi5dxyeoTe73LntZ1cZ0tLyYx6Tn4y6VZH4_XfleA3eog3GgNlHDguCW_2CSl-X11e9OSzdeNogotr1hQYMMIUiAdRIqkkHECwgr7-B72OayqfdEcJwakEKBTZUTbFnJPr7xvHoLee9c6zLp71nWe9jX7155Pvj_wSWwC6A3IphcGl33f_J_YnIfSyQw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2836653800</pqid></control><display><type>article</type><title>Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways</title><source>Springer Nature - Complete Springer Journals</source><source>PubMed Central</source><creator>Tito, Claudia ; Genovese, Ilaria ; Giamogante, Flavia ; Benedetti, Anna ; Miglietta, Selenia ; Barazzuol, Lucia ; Cristiano, Loredana ; Iaiza, Alessia ; Carolini, Sabatino ; De Angelis, Luciana ; Masciarelli, Silvia ; Nottola, Stefania Annarita ; Familiari, Giuseppe ; Petrozza, Vincenzo ; Lauriola, Mattia ; Tamagnone, Luca ; Ilari, Andrea ; Calì, Tito ; Valdivia, Hector H. ; Valdivia, Carmen R. ; Colotti, Gianni ; Fazi, Francesco</creator><creatorcontrib>Tito, Claudia ; Genovese, Ilaria ; Giamogante, Flavia ; Benedetti, Anna ; Miglietta, Selenia ; Barazzuol, Lucia ; Cristiano, Loredana ; Iaiza, Alessia ; Carolini, Sabatino ; De Angelis, Luciana ; Masciarelli, Silvia ; Nottola, Stefania Annarita ; Familiari, Giuseppe ; Petrozza, Vincenzo ; Lauriola, Mattia ; Tamagnone, Luca ; Ilari, Andrea ; Calì, Tito ; Valdivia, Hector H. ; Valdivia, Carmen R. ; Colotti, Gianni ; Fazi, Francesco</creatorcontrib><description>The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-023-04850-4</identifier><identifier>PMID: 37442828</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Calcium ; Calcium homeostasis ; Calcium signalling ; Cancer ; Cell Biology ; Cell migration ; Cell proliferation ; Drug development ; Drug resistance ; drug therapy ; Epidermal growth factor ; Epidermal growth factor receptors ; Growth factors ; Homeostasis ; Life Sciences ; neoplasms ; Original ; Original Article ; Phosphorylation ; Proteins ; Signal transduction ; Therapeutic targets ; Tumors</subject><ispartof>Cellular and molecular life sciences : CMLS, 2023-08, Vol.80 (8), p.202-202, Article 202</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-9f9bd2b5a7978e9294cc10b0572aa9548a2ad126a56081d62ff19427236b55c53</citedby><cites>FETCH-LOGICAL-c508t-9f9bd2b5a7978e9294cc10b0572aa9548a2ad126a56081d62ff19427236b55c53</cites><orcidid>0000-0003-2910-7912</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/PMC10345051/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10345051/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37442828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tito, Claudia</creatorcontrib><creatorcontrib>Genovese, Ilaria</creatorcontrib><creatorcontrib>Giamogante, Flavia</creatorcontrib><creatorcontrib>Benedetti, Anna</creatorcontrib><creatorcontrib>Miglietta, Selenia</creatorcontrib><creatorcontrib>Barazzuol, Lucia</creatorcontrib><creatorcontrib>Cristiano, Loredana</creatorcontrib><creatorcontrib>Iaiza, Alessia</creatorcontrib><creatorcontrib>Carolini, Sabatino</creatorcontrib><creatorcontrib>De Angelis, Luciana</creatorcontrib><creatorcontrib>Masciarelli, Silvia</creatorcontrib><creatorcontrib>Nottola, Stefania Annarita</creatorcontrib><creatorcontrib>Familiari, Giuseppe</creatorcontrib><creatorcontrib>Petrozza, Vincenzo</creatorcontrib><creatorcontrib>Lauriola, Mattia</creatorcontrib><creatorcontrib>Tamagnone, Luca</creatorcontrib><creatorcontrib>Ilari, Andrea</creatorcontrib><creatorcontrib>Calì, Tito</creatorcontrib><creatorcontrib>Valdivia, Hector H.</creatorcontrib><creatorcontrib>Valdivia, Carmen R.</creatorcontrib><creatorcontrib>Colotti, Gianni</creatorcontrib><creatorcontrib>Fazi, Francesco</creatorcontrib><title>Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium</subject><subject>Calcium homeostasis</subject><subject>Calcium signalling</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Drug development</subject><subject>Drug resistance</subject><subject>drug therapy</subject><subject>Epidermal growth factor</subject><subject>Epidermal growth factor receptors</subject><subject>Growth factors</subject><subject>Homeostasis</subject><subject>Life Sciences</subject><subject>neoplasms</subject><subject>Original</subject><subject>Original Article</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Therapeutic targets</subject><subject>Tumors</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkUtrFTEYhoMotlb_gAsZcONm9Mt1kpVI6Q0KQlUQXIRMJjMnZSYZk5lK_705Pcd6WdhVLt-TN1_yIPQSw1sM0LzLAIBlDYTWwCSHmj1Ch5gRqBU0-PF-LiT5eoCe5XxdaC6JeIoOaMMYkUQeom-fYrI-VHOKU1xcriY_JLP4GKqya02wLlUmdFVywzqaLbFsXHVydlp3bnahc2HZrq6q7IdgRh-GajbL5oe5zc_Rk96M2b3Yj0foy-nJ5-Pz-vLj2cXxh8vacpBLrXrVdqTlplGNdIooZi2GFnhDjFGcSUNMh4kwXIDEnSB9jxUjDaGi5dxyeoTe73LntZ1cZ0tLyYx6Tn4y6VZH4_XfleA3eog3GgNlHDguCW_2CSl-X11e9OSzdeNogotr1hQYMMIUiAdRIqkkHECwgr7-B72OayqfdEcJwakEKBTZUTbFnJPr7xvHoLee9c6zLp71nWe9jX7155Pvj_wSWwC6A3IphcGl33f_J_YnIfSyQw</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Tito, Claudia</creator><creator>Genovese, Ilaria</creator><creator>Giamogante, Flavia</creator><creator>Benedetti, Anna</creator><creator>Miglietta, Selenia</creator><creator>Barazzuol, Lucia</creator><creator>Cristiano, Loredana</creator><creator>Iaiza, Alessia</creator><creator>Carolini, Sabatino</creator><creator>De Angelis, Luciana</creator><creator>Masciarelli, Silvia</creator><creator>Nottola, Stefania Annarita</creator><creator>Familiari, Giuseppe</creator><creator>Petrozza, Vincenzo</creator><creator>Lauriola, Mattia</creator><creator>Tamagnone, Luca</creator><creator>Ilari, Andrea</creator><creator>Calì, Tito</creator><creator>Valdivia, Hector H.</creator><creator>Valdivia, Carmen R.</creator><creator>Colotti, Gianni</creator><creator>Fazi, Francesco</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2910-7912</orcidid></search><sort><creationdate>20230801</creationdate><title>Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways</title><author>Tito, Claudia ; Genovese, Ilaria ; Giamogante, Flavia ; Benedetti, Anna ; Miglietta, Selenia ; Barazzuol, Lucia ; Cristiano, Loredana ; Iaiza, Alessia ; Carolini, Sabatino ; De Angelis, Luciana ; Masciarelli, Silvia ; Nottola, Stefania Annarita ; Familiari, Giuseppe ; Petrozza, Vincenzo ; Lauriola, Mattia ; Tamagnone, Luca ; Ilari, Andrea ; Calì, Tito ; Valdivia, Hector H. ; Valdivia, Carmen R. ; Colotti, Gianni ; Fazi, Francesco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-9f9bd2b5a7978e9294cc10b0572aa9548a2ad126a56081d62ff19427236b55c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium</topic><topic>Calcium homeostasis</topic><topic>Calcium signalling</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Drug development</topic><topic>Drug resistance</topic><topic>drug therapy</topic><topic>Epidermal growth factor</topic><topic>Epidermal growth factor receptors</topic><topic>Growth factors</topic><topic>Homeostasis</topic><topic>Life Sciences</topic><topic>neoplasms</topic><topic>Original</topic><topic>Original Article</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Therapeutic targets</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tito, Claudia</creatorcontrib><creatorcontrib>Genovese, Ilaria</creatorcontrib><creatorcontrib>Giamogante, Flavia</creatorcontrib><creatorcontrib>Benedetti, Anna</creatorcontrib><creatorcontrib>Miglietta, Selenia</creatorcontrib><creatorcontrib>Barazzuol, Lucia</creatorcontrib><creatorcontrib>Cristiano, Loredana</creatorcontrib><creatorcontrib>Iaiza, Alessia</creatorcontrib><creatorcontrib>Carolini, Sabatino</creatorcontrib><creatorcontrib>De Angelis, Luciana</creatorcontrib><creatorcontrib>Masciarelli, Silvia</creatorcontrib><creatorcontrib>Nottola, Stefania Annarita</creatorcontrib><creatorcontrib>Familiari, Giuseppe</creatorcontrib><creatorcontrib>Petrozza, Vincenzo</creatorcontrib><creatorcontrib>Lauriola, Mattia</creatorcontrib><creatorcontrib>Tamagnone, Luca</creatorcontrib><creatorcontrib>Ilari, Andrea</creatorcontrib><creatorcontrib>Calì, Tito</creatorcontrib><creatorcontrib>Valdivia, Hector H.</creatorcontrib><creatorcontrib>Valdivia, Carmen R.</creatorcontrib><creatorcontrib>Colotti, Gianni</creatorcontrib><creatorcontrib>Fazi, Francesco</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</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 Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tito, Claudia</au><au>Genovese, Ilaria</au><au>Giamogante, Flavia</au><au>Benedetti, Anna</au><au>Miglietta, Selenia</au><au>Barazzuol, Lucia</au><au>Cristiano, Loredana</au><au>Iaiza, Alessia</au><au>Carolini, Sabatino</au><au>De Angelis, Luciana</au><au>Masciarelli, Silvia</au><au>Nottola, Stefania Annarita</au><au>Familiari, Giuseppe</au><au>Petrozza, Vincenzo</au><au>Lauriola, Mattia</au><au>Tamagnone, Luca</au><au>Ilari, Andrea</au><au>Calì, Tito</au><au>Valdivia, Hector H.</au><au>Valdivia, Carmen R.</au><au>Colotti, Gianni</au><au>Fazi, Francesco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><stitle>Cell. Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2023-08-01</date><risdate>2023</risdate><volume>80</volume><issue>8</issue><spage>202</spage><epage>202</epage><pages>202-202</pages><artnum>202</artnum><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>37442828</pmid><doi>10.1007/s00018-023-04850-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-2910-7912</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1420-682X |
| ispartof | Cellular and molecular life sciences : CMLS, 2023-08, Vol.80 (8), p.202-202, Article 202 |
| issn | 1420-682X 1420-9071 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10345051 |
| source | Springer Nature - Complete Springer Journals; PubMed Central |
| subjects | Biochemistry Biomedical and Life Sciences Biomedicine Calcium Calcium homeostasis Calcium signalling Cancer Cell Biology Cell migration Cell proliferation Drug development Drug resistance drug therapy Epidermal growth factor Epidermal growth factor receptors Growth factors Homeostasis Life Sciences neoplasms Original Original Article Phosphorylation Proteins Signal transduction Therapeutic targets Tumors |
| title | Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-19T18%3A57%3A39IST&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=Sorcin%20promotes%20migration%20in%20cancer%20and%20regulates%20the%20EGF-dependent%20EGFR%20signaling%20pathways&rft.jtitle=Cellular%20and%20molecular%20life%20sciences%20:%20CMLS&rft.au=Tito,%20Claudia&rft.date=2023-08-01&rft.volume=80&rft.issue=8&rft.spage=202&rft.epage=202&rft.pages=202-202&rft.artnum=202&rft.issn=1420-682X&rft.eissn=1420-9071&rft_id=info:doi/10.1007/s00018-023-04850-4&rft_dat=%3Cproquest_pubme%3E3040424906%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=2836653800&rft_id=info:pmid/37442828&rfr_iscdi=true |