دورية أكاديمية

CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming

التفاصيل البيبلوغرافية
العنوان: CXCL12 secreted by pancreatic stellate cells accelerates gemcitabine resistance of pancreatic cancer by enhancing glycolytic reprogramming
المؤلفون: Xiangyu Lu, Yilei Wu, Rui Cao, Xiaojiong Yu, Jun Gong
المصدر: Animal Cells and Systems, Vol 26, Iss 4, Pp 148-157 (2022)
بيانات النشر: Taylor & Francis Group, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine (General)
LCC:Biology (General)
مصطلحات موضوعية: Pancreatic stellate cells, CXCL12, glycolysis, resistance, pancreatic cancer, Medicine (General), R5-920, Biology (General), QH301-705.5
الوصف: Pancreatic stellate cells (PSCs) are the primary cell components of pancreatic cancer (PC) and are involved in tumor growth, metastasis and resistance. However, the role and the mechanism of PSCs in gemcitabine (GEM) resistance to PC still need more investigation. We found that CXCL12 mRNA and secreted CXCL12 protein were higher in PSCs after GEM treatment. The conditioned medium (CM) from GEM-treated PSCs reduced the GEM sensitivity of PC cells. Blocking of CXCL12 in CM by anti-CXCL12 antibody partly restored the GEM sensitivity of PC cells. Blocking of CXCL12 decreased glucose consumption, lactate production, ECAR, and glycolysis-related gene expression in PC cells. The PI3K/AKT/mTOR pathway was activated by the binding of CXCL12 and CXCR4. Moreover, CXCR4 mRNA and protein expressions in PC cells were increased after GEM treatment. Our results indicated the cross-talk between PSCs and PC cells during GEM chemotherapy. CXCL12 secreted by PSCs reduces GEM sensitivity of PC cells by binding to CXCR4 and activating PI3K/AKT/mTOR-glycolysis pathway in PC. Our findings would lay the foundation for solving GEM resistance in PC.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 19768354
2151-2485
1976-8354
العلاقة: https://doaj.org/toc/1976-8354Test; https://doaj.org/toc/2151-2485Test
DOI: 10.1080/19768354.2022.2091019
الوصول الحر: https://doaj.org/article/c225b42dd0e04f26a8d37fdddedb5d0aTest
رقم الانضمام: edsdoj.225b42dd0e04f26a8d37fdddedb5d0a
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19768354
21512485
DOI:10.1080/19768354.2022.2091019