Loading…

Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance

The identity of cancer stem cells (CSCs) remains an enigma, with the question outstanding of whether CSCs are fixed entities or plastic cell states in response to microenvironmental cues. Recent evidence highlights the power of the tumor microenvironment to dictate CSC functionality and spatiotempor...

Full description

Saved in:
Bibliographic Details
Published in:The international journal of biochemistry & cell biology 2019-04, Vol.109, p.90-104
Main Authors: Brown, Yazmin, Hua, Susan, Tanwar, Pradeep S.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483
cites cdi_FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483
container_end_page 104
container_issue
container_start_page 90
container_title The international journal of biochemistry & cell biology
container_volume 109
creator Brown, Yazmin
Hua, Susan
Tanwar, Pradeep S.
description The identity of cancer stem cells (CSCs) remains an enigma, with the question outstanding of whether CSCs are fixed entities or plastic cell states in response to microenvironmental cues. Recent evidence highlights the power of the tumor microenvironment to dictate CSC functionality and spatiotemporal regulation that gives rise to tumor heterogeneity. This microenvironmental regulation of CSCs parallels that of normal tissues, whereby resident stem cells reside within specialized microenvironments or ‘niches’, which provide the cellular and molecular signals that wire every aspect of stem cell behavior and fate. The extracellular matrix (ECM), along with its sequestered growth factors, is a fundamental component of the stem cell niche. Pathological ECM remodeling is an established hallmark of cancer, with the ECM a key mediator of metastasis and drug resistance. In this review, we discuss the controversial identity of CSCs and new understanding of the impact of tumor microenvironment on CSC function and phenotype. We outline parallels between development, wound repair and cancer to discuss how changes in ECM dynamics influence stem cell function during normal physiological processes and pathological states, as well as the transition between the two in the form of precancerous lesions. We then explore examples illustrating the molecular circuits partnering cancer cells with stromal cells and how this communication involving ECM imparts a CSC phenotype and promotes chemoresistance. Understanding the mechanisms underlying CSC functionality and chemoresistance, along with mathematical modeling approaches and advancing technologies for targeting the undruggable proteome, should open opportunities for cancer breakthroughs in the future.
doi_str_mv 10.1016/j.biocel.2019.02.002
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2185870662</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1357272519300366</els_id><sourcerecordid>2185870662</sourcerecordid><originalsourceid>FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483</originalsourceid><addsrcrecordid>eNp9kE1LxDAQhoMouq7-A5EevbRO0iZtL4Is6wcsiKDnkI-pZtluNcnK-u9N2dWjpxlm3nc-HkIuKBQUqLheFtoNBlcFA9oWwAoAdkAmtKmbnDc1P0x5yeuc1YyfkNMQlgBAOSuPyUkJdVUCryfkeb6NXqUxq81K-axX0btt3qN1KqLNPL6lenTDOhu6zKi1QZ-FiH02WkKm1jYz79gPHoMLceyfkaNOrQKe7-OUvN7NX2YP-eLp_nF2u8hNxZqY21ZQ3epK21po22kBrVC869qyAtNWinPOmOBGGAoaueYUOVhe67LUtqmackqudnM__PC5wRBl78J4lVrjsAmS0SZhACFYklY7qfFDCB47-eFdr_y3pCBHmHIpdzDlCFMCkwlmsl3uN2x0IvJn-qWXBDc7AaY_vxx6GYzDxMA6jyZKO7j_N_wAvUOIEw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2185870662</pqid></control><display><type>article</type><title>Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance</title><source>ScienceDirect Freedom Collection 2022-2024</source><creator>Brown, Yazmin ; Hua, Susan ; Tanwar, Pradeep S.</creator><creatorcontrib>Brown, Yazmin ; Hua, Susan ; Tanwar, Pradeep S.</creatorcontrib><description>The identity of cancer stem cells (CSCs) remains an enigma, with the question outstanding of whether CSCs are fixed entities or plastic cell states in response to microenvironmental cues. Recent evidence highlights the power of the tumor microenvironment to dictate CSC functionality and spatiotemporal regulation that gives rise to tumor heterogeneity. This microenvironmental regulation of CSCs parallels that of normal tissues, whereby resident stem cells reside within specialized microenvironments or ‘niches’, which provide the cellular and molecular signals that wire every aspect of stem cell behavior and fate. The extracellular matrix (ECM), along with its sequestered growth factors, is a fundamental component of the stem cell niche. Pathological ECM remodeling is an established hallmark of cancer, with the ECM a key mediator of metastasis and drug resistance. In this review, we discuss the controversial identity of CSCs and new understanding of the impact of tumor microenvironment on CSC function and phenotype. We outline parallels between development, wound repair and cancer to discuss how changes in ECM dynamics influence stem cell function during normal physiological processes and pathological states, as well as the transition between the two in the form of precancerous lesions. We then explore examples illustrating the molecular circuits partnering cancer cells with stromal cells and how this communication involving ECM imparts a CSC phenotype and promotes chemoresistance. Understanding the mechanisms underlying CSC functionality and chemoresistance, along with mathematical modeling approaches and advancing technologies for targeting the undruggable proteome, should open opportunities for cancer breakthroughs in the future.</description><identifier>ISSN: 1357-2725</identifier><identifier>EISSN: 1878-5875</identifier><identifier>DOI: 10.1016/j.biocel.2019.02.002</identifier><identifier>PMID: 30743057</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>Breast cancer ; Cancer ; Chemoresistance ; CSCs ; Drug resistance ; ECM ; EMT ; Epidermolysis bullosa ; Extracellular matrix ; Glioblastoma ; Ovarian cancer ; Squamous cell carcinoma ; Stem cells ; Tumor microenvironment</subject><ispartof>The international journal of biochemistry &amp; cell biology, 2019-04, Vol.109, p.90-104</ispartof><rights>2019 Elsevier Ltd</rights><rights>Copyright © 2019 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483</citedby><cites>FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483</cites><orcidid>0000-0002-6416-7315</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30743057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, Yazmin</creatorcontrib><creatorcontrib>Hua, Susan</creatorcontrib><creatorcontrib>Tanwar, Pradeep S.</creatorcontrib><title>Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance</title><title>The international journal of biochemistry &amp; cell biology</title><addtitle>Int J Biochem Cell Biol</addtitle><description>The identity of cancer stem cells (CSCs) remains an enigma, with the question outstanding of whether CSCs are fixed entities or plastic cell states in response to microenvironmental cues. Recent evidence highlights the power of the tumor microenvironment to dictate CSC functionality and spatiotemporal regulation that gives rise to tumor heterogeneity. This microenvironmental regulation of CSCs parallels that of normal tissues, whereby resident stem cells reside within specialized microenvironments or ‘niches’, which provide the cellular and molecular signals that wire every aspect of stem cell behavior and fate. The extracellular matrix (ECM), along with its sequestered growth factors, is a fundamental component of the stem cell niche. Pathological ECM remodeling is an established hallmark of cancer, with the ECM a key mediator of metastasis and drug resistance. In this review, we discuss the controversial identity of CSCs and new understanding of the impact of tumor microenvironment on CSC function and phenotype. We outline parallels between development, wound repair and cancer to discuss how changes in ECM dynamics influence stem cell function during normal physiological processes and pathological states, as well as the transition between the two in the form of precancerous lesions. We then explore examples illustrating the molecular circuits partnering cancer cells with stromal cells and how this communication involving ECM imparts a CSC phenotype and promotes chemoresistance. Understanding the mechanisms underlying CSC functionality and chemoresistance, along with mathematical modeling approaches and advancing technologies for targeting the undruggable proteome, should open opportunities for cancer breakthroughs in the future.</description><subject>Breast cancer</subject><subject>Cancer</subject><subject>Chemoresistance</subject><subject>CSCs</subject><subject>Drug resistance</subject><subject>ECM</subject><subject>EMT</subject><subject>Epidermolysis bullosa</subject><subject>Extracellular matrix</subject><subject>Glioblastoma</subject><subject>Ovarian cancer</subject><subject>Squamous cell carcinoma</subject><subject>Stem cells</subject><subject>Tumor microenvironment</subject><issn>1357-2725</issn><issn>1878-5875</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kE1LxDAQhoMouq7-A5EevbRO0iZtL4Is6wcsiKDnkI-pZtluNcnK-u9N2dWjpxlm3nc-HkIuKBQUqLheFtoNBlcFA9oWwAoAdkAmtKmbnDc1P0x5yeuc1YyfkNMQlgBAOSuPyUkJdVUCryfkeb6NXqUxq81K-axX0btt3qN1KqLNPL6lenTDOhu6zKi1QZ-FiH02WkKm1jYz79gPHoMLceyfkaNOrQKe7-OUvN7NX2YP-eLp_nF2u8hNxZqY21ZQ3epK21po22kBrVC869qyAtNWinPOmOBGGAoaueYUOVhe67LUtqmackqudnM__PC5wRBl78J4lVrjsAmS0SZhACFYklY7qfFDCB47-eFdr_y3pCBHmHIpdzDlCFMCkwlmsl3uN2x0IvJn-qWXBDc7AaY_vxx6GYzDxMA6jyZKO7j_N_wAvUOIEw</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Brown, Yazmin</creator><creator>Hua, Susan</creator><creator>Tanwar, Pradeep S.</creator><general>Elsevier Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6416-7315</orcidid></search><sort><creationdate>20190401</creationdate><title>Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance</title><author>Brown, Yazmin ; Hua, Susan ; Tanwar, Pradeep S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Breast cancer</topic><topic>Cancer</topic><topic>Chemoresistance</topic><topic>CSCs</topic><topic>Drug resistance</topic><topic>ECM</topic><topic>EMT</topic><topic>Epidermolysis bullosa</topic><topic>Extracellular matrix</topic><topic>Glioblastoma</topic><topic>Ovarian cancer</topic><topic>Squamous cell carcinoma</topic><topic>Stem cells</topic><topic>Tumor microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, Yazmin</creatorcontrib><creatorcontrib>Hua, Susan</creatorcontrib><creatorcontrib>Tanwar, Pradeep S.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The international journal of biochemistry &amp; cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Yazmin</au><au>Hua, Susan</au><au>Tanwar, Pradeep S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance</atitle><jtitle>The international journal of biochemistry &amp; cell biology</jtitle><addtitle>Int J Biochem Cell Biol</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>109</volume><spage>90</spage><epage>104</epage><pages>90-104</pages><issn>1357-2725</issn><eissn>1878-5875</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>The identity of cancer stem cells (CSCs) remains an enigma, with the question outstanding of whether CSCs are fixed entities or plastic cell states in response to microenvironmental cues. Recent evidence highlights the power of the tumor microenvironment to dictate CSC functionality and spatiotemporal regulation that gives rise to tumor heterogeneity. This microenvironmental regulation of CSCs parallels that of normal tissues, whereby resident stem cells reside within specialized microenvironments or ‘niches’, which provide the cellular and molecular signals that wire every aspect of stem cell behavior and fate. The extracellular matrix (ECM), along with its sequestered growth factors, is a fundamental component of the stem cell niche. Pathological ECM remodeling is an established hallmark of cancer, with the ECM a key mediator of metastasis and drug resistance. In this review, we discuss the controversial identity of CSCs and new understanding of the impact of tumor microenvironment on CSC function and phenotype. We outline parallels between development, wound repair and cancer to discuss how changes in ECM dynamics influence stem cell function during normal physiological processes and pathological states, as well as the transition between the two in the form of precancerous lesions. We then explore examples illustrating the molecular circuits partnering cancer cells with stromal cells and how this communication involving ECM imparts a CSC phenotype and promotes chemoresistance. Understanding the mechanisms underlying CSC functionality and chemoresistance, along with mathematical modeling approaches and advancing technologies for targeting the undruggable proteome, should open opportunities for cancer breakthroughs in the future.</abstract><cop>Netherlands</cop><pub>Elsevier Ltd</pub><pmid>30743057</pmid><doi>10.1016/j.biocel.2019.02.002</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-6416-7315</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 1357-2725
ispartof The international journal of biochemistry & cell biology, 2019-04, Vol.109, p.90-104
issn 1357-2725
1878-5875
language eng
recordid cdi_proquest_miscellaneous_2185870662
source ScienceDirect Freedom Collection 2022-2024
subjects Breast cancer
Cancer
Chemoresistance
CSCs
Drug resistance
ECM
EMT
Epidermolysis bullosa
Extracellular matrix
Glioblastoma
Ovarian cancer
Squamous cell carcinoma
Stem cells
Tumor microenvironment
title Extracellular matrix-mediated regulation of cancer stem cells and chemoresistance
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T09%3A37%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Extracellular%20matrix-mediated%20regulation%20of%20cancer%20stem%20cells%20and%20chemoresistance&rft.jtitle=The%20international%20journal%20of%20biochemistry%20&%20cell%20biology&rft.au=Brown,%20Yazmin&rft.date=2019-04-01&rft.volume=109&rft.spage=90&rft.epage=104&rft.pages=90-104&rft.issn=1357-2725&rft.eissn=1878-5875&rft_id=info:doi/10.1016/j.biocel.2019.02.002&rft_dat=%3Cproquest_cross%3E2185870662%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c428t-d961b9b4bd76bdfb6096a5ff9340c94a5552265c6c10be5b51e50d57b33bd8483%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2185870662&rft_id=info:pmid/30743057&rfr_iscdi=true