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Direct cell-to-cell transfer in stressed tumor microenvironment aggravates tumorigenic or metastatic potential in pancreatic cancer
DC Field | Value | Language |
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dc.contributor.author | Jang, Giyong | - |
dc.contributor.author | Oh, Jaeik | - |
dc.contributor.author | Jun, Eunsung | - |
dc.contributor.author | Lee, Jieun | - |
dc.contributor.author | Kwon, Jee Young | - |
dc.contributor.author | Kim, Jaesang | - |
dc.contributor.author | Lee, Sang-Hyuk | - |
dc.contributor.author | Kim, Song Cheol | - |
dc.contributor.author | Cho, Sung Yup | - |
dc.contributor.author | Lee, Charles | - |
dc.date.accessioned | 2024-05-16T01:37:33Z | - |
dc.date.available | 2024-05-16T01:37:33Z | - |
dc.date.created | 2022-11-21 | - |
dc.date.created | 2022-11-21 | - |
dc.date.created | 2022-11-21 | - |
dc.date.issued | 2022-10 | - |
dc.identifier.citation | npj Genomic Medicine, Vol.7 No.1, p. 63 | - |
dc.identifier.issn | 2056-7944 | - |
dc.identifier.uri | https://hdl.handle.net/10371/202729 | - |
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 (CD44(high)/SLC16A1(high)) 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 CD44(low)/SLC16A1(low) 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. | - |
dc.language | 영어 | - |
dc.publisher | Nature Publishing Group | The Center of Excellence in Genomic Medicine Research at King Abdulaziz University | - |
dc.title | Direct cell-to-cell transfer in stressed tumor microenvironment aggravates tumorigenic or metastatic potential in pancreatic cancer | - |
dc.type | Article | - |
dc.identifier.doi | 10.1038/s41525-022-00333-w | - |
dc.citation.journaltitle | npj Genomic Medicine | - |
dc.identifier.wosid | 000876121900001 | - |
dc.identifier.scopusid | 2-s2.0-85140878573 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 63 | - |
dc.citation.volume | 7 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Cho, Sung Yup | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | MONOCARBOXYLATE TRANSPORTER 1 | - |
dc.subject.keywordPlus | STEM-CELLS | - |
dc.subject.keywordPlus | STELLATE CELLS | - |
dc.subject.keywordPlus | BREAST-CANCER | - |
dc.subject.keywordPlus | MCT1 | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | EXOSOMES | - |
dc.subject.keywordPlus | INVASION | - |
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