Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 윤채옥 | - |
dc.date.accessioned | 2019-10-17T01:57:37Z | - |
dc.date.available | 2019-10-17T01:57:37Z | - |
dc.date.issued | 2019-09 | - |
dc.identifier.citation | CANCER LETTERS, v. 459, Page. 15-29 | en_US |
dc.identifier.issn | 0304-3835 | - |
dc.identifier.issn | 1872-7980 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S0304383519303283?via%3Dihub | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/111169 | - |
dc.description.abstract | Pancreatic cancer is a highly lethal disease. Excessive accumulation of tumor extracellular matrix (ECM) and epithelial-to-mesenchymal transition (EMT) phenotype are two main contributors to drug resistance in desmoplastic pancreatic tumors. To overcome desmoplasia and chemoresistance of pancreatic cancer, we utilized an oncolytic adenovirus (Ad) co-expressing decorin and soluble Wnt decoy receptor (HEmT-DCN/sLRP6). An orthotopic pancreatic xenograft tumor model was established in athymic nude mice using Mia PaCa-2 cells, and the antimetastatic and antitumor efficacy of systemically administered HEmT-DCN/sLRP6 was evaluated. Immunohistochemical analysis of tumor tissues was performed to assess ECM degradation, induction of apoptosis, viral dispersion, and inhibition of the Wnta-catenin signaling pathway. HEmT-DCN/sLRP6 effectively degraded tumor ECM and inhibited EMT, leading to enhanced viral distribution, induction of apoptosis, and attenuation of tumor cell proliferation in tumor tissue. HEmT-DCN/sLRP6 prevented metastasis of pancreatic cancer. Importantly, HEmT-DCN/sLRP6 sensitized pancreatic tumor to gemcitabine treatment. Furthermore, HEmT-DCN/sLRP6 augmented drug penetration and dispersion within pancreatic tumor xenografts and patient derived tumor spheroids. Collectively, these results illustrate that HEmT-DCN/sLRP6 can enhance the dispersion of both oncolytic Ad and a chemotherapeutic agent in chemoresistant and desmoplastic pancreatic tumor, effectively overcoming the preexisting limitations of standard treatments. | en_US |
dc.description.sponsorship | This work was supported by grant from the National Research Foundation of Korea (2016M3A9B5942352; Dr. C-O Yun) and the Research Fund of Hanyang University (HY-2011-G-201100000001880; Dr. C-O Yun). | en_US |
dc.language.iso | en | en_US |
dc.publisher | ELSEVIER IRELAND LTD | en_US |
dc.subject | Decorin | en_US |
dc.subject | sLRP6E1E2 | en_US |
dc.subject | Oncolytic adenovirus | en_US |
dc.subject | Pancreatic cancer | en_US |
dc.subject | Metastasis | en_US |
dc.subject | xtracellular matrix | en_US |
dc.subject | Chemosensitivity | en_US |
dc.title | Oncolytic Ad co-expressing decorin and Wnt decoy receptor overcomes chemoresistance of desmoplastic tumor through degradation of ECM and inhibition of EMT | en_US |
dc.type | Article | en_US |
dc.relation.volume | 459 | - |
dc.identifier.doi | 10.1016/j.canlet.2019.05.033 | - |
dc.relation.page | 15-29 | - |
dc.relation.journal | CANCER LETTERS | - |
dc.contributor.googleauthor | Li, Yan | - |
dc.contributor.googleauthor | Hong, JinWoo | - |
dc.contributor.googleauthor | Jung, Bo-Kyeong | - |
dc.contributor.googleauthor | Oh, Eonju | - |
dc.contributor.googleauthor | Yun, Chae-Ok | - |
dc.relation.code | 2019003359 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF ENGINEERING[S] | - |
dc.sector.department | DEPARTMENT OF BIOENGINEERING | - |
dc.identifier.pid | chaeok | - |
dc.identifier.orcid | https://orcid.org/0000-0002-9466-4531 | - |
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