Background: In the tumor environment, malignant characteristics of cancer cells are promoted by stromal cells under hypoxia. It is unknown whether lysophosphatidic acid (LPA) receptor-mediated signaling is involved in the regulation of cellular functions by endothelial cells in pancreatic cancer cells under hypoxic conditions.
Methods: Pancreatic cancer (PANC-1) cells were co-cultured with endothelial (F2) cells and F2 cell supernatants at 21% and 1% O. The Cell Culture Insert was used to assess the cell motile activity. The cell growth and viability to cisplatin (CDDP) were measured, using the Cell Counting Kit-8.
Results: LPA receptor expression levels were changed in PANC-1 cells co-cultured with F2 cells at 21% and 1% O. The cell motile activities of PANC-1 cells co-cultured with F2 cells at 21% and 1% O were markedly elevated, compared with PANC-1 cells alone. The cell viabilities to CDDP of PANC-1 cells co-cultured with F2 cell supernatants at 21% and 1% O were regulated by the activation of LPA receptors.
Conclusion: These results suggest that LPA receptor-mediated signaling plays an important role in the modulation of pancreatic cancer cell functions by endothelial cells under hypoxic conditions.
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http://dx.doi.org/10.1016/j.prp.2024.155192 | DOI Listing |
Acta Pharmacol Sin
January 2025
State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Sustainable Chemical Transformations, Frontiers Science Center for New Organic Matter, College of Chemistry, Nankai University, Tianjin, 300350, China.
Hypoxia is a key feature of the tumor microenvironment that leads to the failure of many chemotherapies and induces more aggressive and resistant cancer phenotypes. Up to date, there are very few compounds and treatments that can target hypoxia. BE-43547A from Streptomyces sp.
View Article and Find Full Text PDFChemMedChem
January 2025
Kobe Pharmaceutical University: Kobe Yakka Daigaku, Laboratory of Microbial Chemistry, 4-19-1 Motoyamakita, Higashinada, 6588558, Kobe, JAPAN.
The antiausterity strategy in anticancer drug discovery has attracted much attention as a way to exterminate cancer cells under nutrient deprived conditions which are commonly found in solid tumors. These tumors under low nutrient stress are known to be malignant and often resist conventional drug therapy. As a potential drug candidate, we focused on the meroterpenoid natural product callistrilone O which has demonstrated extremely potent antiausterity properties toward PANC-1 pancreatic carcinoma in vitro.
View Article and Find Full Text PDFBioeng Transl Med
January 2025
Department of Chemical and Biomolecular Engineering Yonsei University Seoul South Korea.
This study presents a novel in vitro bilayer 3D co-culture platform designed to obtain cancer-associated fibroblasts (CAFs)-like cells. The platform consists of a bilayer hydrogel structure with a collagen/polyethylene glycol (PEG) hydrogel for fibroblasts as the upper layer and an alginate hydrogel for tumor cells as the lower layer. The platform enabled paracrine interactions between fibroblasts and cancer cells, which allowed for selective retrieval of activated fibroblasts through collagenase treatment for further study.
View Article and Find Full Text PDFBiomater Adv
January 2025
National University of Science and Technology MISIS, 119049, Leninskiy pr. 4, Moscow, Russia. Electronic address:
Cancer, one of the world's deadliest diseases, is expected to claim an estimated 16 million lives by 2040. Three-dimensional (3D) models of cancer have become invaluable tools for the study of tumor biology and the development of new therapies. The tumor microenvironment (TME) is a determinant of tumor progression and has implications for clinical therapies.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Laboratory of Chronobiology, Institute of Biosciences and Applications (IBA), National Centre for Scientific Research (NCSR) "Demokritos", 153 41 Aghia Paraskevi, Greece.
: Pancreatic Ductal Adeno-Carcinoma (PDAC) is a highly aggressive cancer, with limited treatment options. Disruption of the circadian clock, which regulates key cellular processes, has been implicated in PDAC initiation and progression. Hence, targeting circadian clock components may offer new therapeutic opportunities for the disease.
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