Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이상혁 | * |
dc.contributor.author | 김재상 | * |
dc.contributor.author | Charles Lee | * |
dc.contributor.author | 장기용 | * |
dc.contributor.author | 이지은 | * |
dc.date.accessioned | 2023-01-04T16:31:11Z | - |
dc.date.available | 2023-01-04T16:31:11Z | - |
dc.date.issued | 2022 | * |
dc.identifier.issn | 2056-7944 | * |
dc.identifier.other | OAK-32588 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/262998 | - |
dc.description.abstract | Pancreatic cancer exhibits a characteristic tumor microenvironment (TME) due to enhanced fibrosis and hypoxia and is particularly resistant to conventional chemotherapy. However, the molecular mechanisms underlying TME-associated treatment resistance in pancreatic cancer are not fully understood. Here, we developed an in vitro TME mimic system comprising pancreatic cancer cells, fibroblasts and immune cells, and a stress condition, including hypoxia and gemcitabine. Cells with high viability under stress showed evidence of increased direct cell-to-cell transfer of biomolecules. The resulting derivative cells (CD44high/SLC16A1high) were similar to cancer stem cell-like-cells (CSCs) with enhanced anchorage-independent growth or invasiveness and acquired metabolic reprogramming. Furthermore, CD24 was a determinant for transition between the tumorsphere formation or invasive properties. Pancreatic cancer patients with CD44low/SLC16A1low expression exhibited better prognoses compared to other groups. Our results suggest that crosstalk via direct cell-to-cell transfer of cellular components foster chemotherapy-induced tumor evolution and that targeting of CD44 and MCT1(encoded by SLC16A1) may be useful strategy to prevent recurrence of gemcitabine-exposed pancreatic cancers. © 2022, The Author(s). | * |
dc.language | English | * |
dc.publisher | Nature Research | * |
dc.title | Direct cell-to-cell transfer in stressed tumor microenvironment aggravates tumorigenic or metastatic potential in pancreatic cancer | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 7 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | npj Genomic Medicine | * |
dc.identifier.doi | 10.1038/s41525-022-00333-w | * |
dc.identifier.wosid | WOS:000876121900001 | * |
dc.identifier.scopusid | 2-s2.0-85140878573 | * |
dc.author.google | Jang G. | * |
dc.author.google | Oh J. | * |
dc.author.google | Jun E. | * |
dc.author.google | Lee J. | * |
dc.author.google | Kwon J.Y. | * |
dc.author.google | Kim J. | * |
dc.author.google | Lee S.-H. | * |
dc.author.google | Kim S.C. | * |
dc.author.google | Cho S.-Y. | * |
dc.author.google | Lee C. | * |
dc.contributor.scopusid | 이상혁(57212112170) | * |
dc.contributor.scopusid | 김재상(8643335800) | * |
dc.contributor.scopusid | Charles Lee(23980489900;57290864600) | * |
dc.contributor.scopusid | 장기용(7102646075) | * |
dc.contributor.scopusid | 이지은(57203144672) | * |
dc.date.modifydate | 20240415122632 | * |