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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
dc.contributor.authorJang, Giyong-
dc.contributor.authorOh, Jaeik-
dc.contributor.authorJun, Eunsung-
dc.contributor.authorLee, Jieun-
dc.contributor.authorKwon, Jee Young-
dc.contributor.authorKim, Jaesang-
dc.contributor.authorLee, Sang-Hyuk-
dc.contributor.authorKim, Song Cheol-
dc.contributor.authorCho, Sung Yup-
dc.contributor.authorLee, Charles-
dc.date.accessioned2024-05-16T01:37:33Z-
dc.date.available2024-05-16T01:37:33Z-
dc.date.created2022-11-21-
dc.date.created2022-11-21-
dc.date.created2022-11-21-
dc.date.issued2022-10-
dc.identifier.citationnpj Genomic Medicine, Vol.7 No.1, p. 63-
dc.identifier.issn2056-7944-
dc.identifier.urihttps://hdl.handle.net/10371/202729-
dc.description.abstractPancreatic 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.language영어-
dc.publisherNature Publishing Group | The Center of Excellence in Genomic Medicine Research at King Abdulaziz University-
dc.titleDirect cell-to-cell transfer in stressed tumor microenvironment aggravates tumorigenic or metastatic potential in pancreatic cancer-
dc.typeArticle-
dc.identifier.doi10.1038/s41525-022-00333-w-
dc.citation.journaltitlenpj Genomic Medicine-
dc.identifier.wosid000876121900001-
dc.identifier.scopusid2-s2.0-85140878573-
dc.citation.number1-
dc.citation.startpage63-
dc.citation.volume7-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorCho, Sung Yup-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusMONOCARBOXYLATE TRANSPORTER 1-
dc.subject.keywordPlusSTEM-CELLS-
dc.subject.keywordPlusSTELLATE CELLS-
dc.subject.keywordPlusBREAST-CANCER-
dc.subject.keywordPlusMCT1-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusIDENTIFICATION-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusEXOSOMES-
dc.subject.keywordPlusINVASION-
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Research Area Cancer genomics, Drug resistance, Targeted therapeutics

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