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dc.contributor.authorKAUSHIK, NEHA-
dc.date.accessioned2019-07-10T07:08:01Z-
dc.date.available2019-07-10T07:08:01Z-
dc.date.issued2019-01-
dc.identifier.citationARCHIVES OF PHARMACAL RESEARCH, v. 42, NO. 1, Page. 40-47en_US
dc.identifier.issn1976-3786-
dc.identifier.issn0253-6269-
dc.identifier.urihttps://link.springer.com/article/10.1007%2Fs12272-018-1097-0-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/107280-
dc.description.abstractCancer is a systemic disease in which neoplastic cells interact with multiple types of non-neoplastic stromal cells as well as non-cellular components. The extracellular matrix (ECM) is a non-cellular component that is aberrantly regulated in many types of tumor microenvironments. Since the ECM generally maintains the tissue structure and provides mechanical forces in the tumor microenvironment, it has been simply assumed to act as a physical barrier for cancer metastasis and have a passive role in cancer progression. However, a substantial body of evidence has suggested that ECM remodeling influences many aspects of cancer cell behaviors and its importance has attracted attention in cancer biology. Abnormal ECM affects cancer progression through several ways such as inducing hypoxia, immune cells interaction by promoting mesenchymal shift and cell transformation. Accordingly, in this review we summarize and discusses the role of the ECM in modulating epithelial cells and surrounding stomatal cell components and considers its prospects in cancer biology.en_US
dc.description.sponsorshipThis work was supported by the National Research Foundation (NRF) and Ministry of Science, ICT and Future Planning, Korean government, through its National Nuclear Technology Program (2016R1E1A1A01942075).en_US
dc.language.isoenen_US
dc.publisherPHARMACEUTICAL SOC KOREAen_US
dc.subjectExtracellular matrixen_US
dc.subjectMetastatic canceren_US
dc.subjectCancer stem cellsen_US
dc.subjectHypoxiaen_US
dc.subjectImmune cellsen_US
dc.titleProinvasive extracellular matrix remodeling for tumor progression.en_US
dc.typeArticleen_US
dc.relation.no1-
dc.relation.volume42-
dc.identifier.doi10.1007/s12272-018-1097-0-
dc.relation.page40-47-
dc.relation.journalARCHIVES OF PHARMACAL RESEARCH-
dc.contributor.googleauthorKaushik, Neha-
dc.contributor.googleauthorKim, Seungmo-
dc.contributor.googleauthorSuh, Yongjoon-
dc.contributor.googleauthorLee, Su-Jae-
dc.relation.code2019040759-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentTHE RESEARCH INSTITUTE FOR NATURAL SCIENCES-
dc.identifier.pidneha1987-
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