scholarly journals mRNA expression profiles obtained from microdissected pancreatic cancer cells can predict patient survival

Oncotarget ◽  
2017 ◽  
Vol 8 (62) ◽  
pp. 104796-104805
Author(s):  
Ana-Barbara García-García ◽  
M. Carmen Gómez-Mateo ◽  
Rebeca Hilario ◽  
Pilar Rentero-Garrido ◽  
Alvaro Martínez-Domenech ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Patient Survival ◽  
Expression Profiles ◽  
Pancreatic Cancer Cells

Galectin-3 is modulated in pancreatic cancer cells under hypoxia and nutrient deprivation

2020 ◽  
Vol 401 (10) ◽  
pp. 1153-1165 ◽  
Author(s):  
Antônio F. da Silva Filho ◽  
Lucas B. Tavares ◽  
Maira G. R. Pitta ◽  
Eduardo I. C. Beltrão ◽  
Moacyr J. B. M. Rêgo
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Ductal Adenocarcinoma ◽  
Reverse Transcription Pcr ◽  
Pancreatic Cancer Cells ◽  
Through Flow ◽  
Galectin 3

AbstractPancreatic ductal adenocarcinoma is one of the most aggressive tumors with a microenvironment marked by hypoxia and starvation. Galectin-3 has been evaluated in solid tumors and seems to present both pro/anti-tumor effects. So, this study aims to characterize the expression of Galectin-3 from pancreatic tumor cells and analyze its influence for cell survive and motility in mimetic microenvironment. For this, cell cycle and cell death were accessed through flow cytometry. Characterization of inside and outside Galectin-3 was performed through Real-Time Quantitative Reverse Transcription PCR (qRT-PCR), immunofluorescence, Western blot, and ELISA. Consequences of Galectin-3 extracellular inhibition were investigated using cell death and scratch assays. PANC-1 showed increased Galectin-3 mRNA expression when cultivated in hypoxia for 24 and 48 h. After 24 h in simultaneously hypoxic/deprived incubation, PANC-1 shows increased Galectin-3 protein and secreted levels. For Mia PaCa-2, cultivation in deprivation was determinant for the increasing in Galectin-3 mRNA expression. When cultivated in simultaneously hypoxic/deprived condition, Mia PaCa-2 also presented increasing for the Galectin-3 secreted levels. Treatment of PANC-1 cells with lactose increased the death rate when cells were incubated simultaneously hypoxic/deprived condition. Therefore, it is possible to conclude that the microenvironmental conditions modulate the Galectin-3 expression on the transcriptional and translational levels for pancreatic cancer cells.

scholarly journals S100A4 mRNA expression level is a predictor of radioresistance of pancreatic cancer cells

2013 ◽  
Vol 30 (4) ◽  
pp. 1601-1608 ◽  
Author(s):  
SHINGO KOZONO ◽  
KENOKI OHUCHIDA ◽  
TAKAO OHTSUKA ◽  
LIN CUI ◽  
DAIKI EGUCHI ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Expression Level ◽  
Mrna Expression Level ◽  
Pancreatic Cancer Cells ◽  
S100a4 Mrna

scholarly journals Curcumin (diferuloylmethane) alters the expression profiles of microRNAs in human pancreatic cancer cells

2008 ◽  
Vol 7 (3) ◽  
pp. 464-473 ◽  
Author(s):  
Michael Sun ◽  
Zeev Estrov ◽  
Yuan Ji ◽  
Kevin R. Coombes ◽  
David H. Harris ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

scholarly journals Impact of LMWH and Specific Factor Xa Inhibitors, Apixaban and Fondaparinux, on Cancer Cell Biology and Procoagulant Properties of Cancer Microenvironment

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2136-2136
Author(s):  
Huong Chi Mai Tran ◽  
Rania Amrane ◽  
Elisabeth Mbemba ◽  
Michele Sabbah ◽  
Ismail Elalamy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Biology ◽  
Thrombin Generation ◽  
Antithrombotic Agents ◽  
Pancreatic Cancer Cells ◽  
The Impact

Abstract Background Cancer patients with venous thromboembolism (VTE) or at risk of VTE are treated with antithrombotic agents. Cancer cells express procoagulant properties and induce hypercoagulability in the microenvironment, that could impact the efficiency of the antithrombotic agents. Aims In the present study, we investigated the interaction between antithrombotic agents with pancreatic cancer cells, as well as with their microenvironment. The impact of apixaban, fondaparinux, enoxaparin and tinzaparin on the procoagulant properties of pancreatic cancer cells BXPC3 was examinated. Reciprocally, we also investigated the impact of BXPC3 on the potency of these antithrombotic agents. Methods BXPC3 cells (400 cells/μl) were exposed for 48 hours to apixaban (2 µg/ml), fondaparinux (2 µg/ml), enoxaparin, tinzaparin (2 anti-Xa IU/ml) or NaCL (control). Then, conditioned media (CM) and BXPC3 cells were harvested, separated and put in contact with normal platelet-poor plasma (PPP). Subsequently, thrombin generation (TG) was assessed using Thrombogram-Thrombinoscope® assay (Diagnostica Stago). Cells' viability was also assessed with the MTT assay. Gene expression for Tissue Factor (TF), Vascular Endothelial Growth Factor (VEGF), Thrombospondin 1 (THSB1) was assessed with RT-qPCR at the cells exposed or not to the antithrombotic agents. Expression of TF protein and activity of cancer cells was assessed using ELISA method. Residual anti-Xa activity in CM was measured using specific amidolytic assays for each antithrombotic agent. Results Apixaban, fondaparinux, enoxaparin, and tinzaparin significantly reduced cell viability by 25%, 12%, 14%, and 11% respectively. In the control experiment non treated BXPC3 cells enhanced TG. Pre-treatment of BXPC3 with the antithrombotic agents did not significantly modify their capacity to trigger and enhance TG. Among the studied agents only apixaban resulted in significant decrease of TF mRNA expression. However, protein expression of TF was not significantly modified by any of the antithrombotic agents. VEGF's mRNA expression was significantly decreased by fondaparinux and enoxaparin. THBS1's mRNA expression was significantly increased by apixaban. The concentrations of the anti-Xa activity of fondaparinux, enoxaparin and tinzaparin in the CM obtained at 48h after exposure of cells were reduced by 27%, 48% and 26% respectively as compared to those initially added in the culture medium. In contrast, the concentration of apixaban in the CM did not significantly change. The CM obtained by cells exposed to apixaban, fondaparinux, enoxaparin and tinzaparin inhibited TG by 70%, 30%, 40% and 90% respectively. Conclusion. Antithrombotic agents reduced the viability of BXPC3 cells. Among the studied agents, apixaban had the most pronounced effect on cells' viability. The antithrombotic agents had a potential downregulating effect on the proangiogenetic properties of BXPC3 via the decrease of VEGF gene expression (fondaparinux and enoxaparin) and enhancement of THBS1 gene expression (apixaban). Nevertheless, preincubation of BXPC3 with the antithrombotic agents did not alter the expression of TF protein and their effect on thrombin generation. Moreover, BXPCE exerted a "degradation" effect on LMWH and fondaparinux. Apixaban appeared to escape from this effect of the cancer cells. A significant inhibitory effect on thrombin generation was exerted by the residual concentrations of the antithrombotic agents in the microenvironment of cancer cells. The ensemble of these data highlight for the first time that the presence of antithrombotic agents in cancer cell microenvironment alters the biology of cancer cells and offer a constant antithrombotic effect in the microenvironment. Disclosures No relevant conflicts of interest to declare.

scholarly journals Electrochemotherapy Causes Caspase-Independent Necrotic-Like Death in Pancreatic Cancer Cells

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1177 ◽  
Author(s):  
Philana Fernandes ◽  
Tracey R. O’Donovan ◽  
Sharon L. McKenna ◽  
Patrick F. Forde
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Patient Survival ◽  
Morphological Changes ◽  
Drug Uptake ◽  
Cancer Therapies ◽  
Pancreatic Cancer Cells ◽  
Membrane Porosity

Pancreatic cancer represents a major challenge in oncology. Poor permeability of the pancreas and resistance to currently available therapies are impediments to improved patient survival. By transiently increasing cell membrane porosity and increasing drug uptake, Electrochemotherapy (ECT) has the potential to overcome these issues. In this study, we have evaluated the response of human and murine pancreatic cancer cells, in vitro, to electroporation in combination with Bleomycin, Cisplatin, or Oxaliplatin (ECT). The cytotoxic actions of all three drugs are potentiated when combined with electroporation in these cells. The biochemical and morphological changes post ECT are associated with immunogenic cell death that occurs with necroptosis rather than apoptosis. Moreover, ECT-induced cell death is rescued by Nec-1 suggesting that necroptosis may play a role in cell death mediated by cancer therapies.

Metformin alters the expression profiles of microRNAs in human pancreatic cancer cells

2012 ◽  
Vol 96 (2) ◽  
pp. 187-195 ◽  
Author(s):  
Weiguang Li ◽  
Yaozong Yuan ◽  
Liya Huang ◽  
Minmin Qiao ◽  
Yongping Zhang
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

scholarly journals Restoration of miR-340 controls pancreatic cancer cellCD47expression to promote macrophage phagocytosis and enhance antitumor immunity

2020 ◽  
Vol 8 (1) ◽  
pp. e000253 ◽  
Author(s):  
Qing Xi ◽  
Jieyou Zhang ◽  
Guangze Yang ◽  
Lijuan Zhang ◽  
Ying Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
T Cells ◽  
Cancer Cells ◽  
Antitumor Immunity ◽  
Patient Survival ◽  
Regulatory Protein ◽  
Luciferase Reporter ◽  
Pancreatic Cancer Cells ◽  
Macrophage Phagocytosis

BackgroundImmune checkpoint blockade has emerged as a potential cancer immunotherapy. The “don’t eat me” signalCD47in cancer cells binds signal regulatory protein-α on macrophages and prevents their phagocytosis. The role of miR-340 in pancreatic ductal adenocarcinoma (PDAC), especially in tumor immunity, has not been explored. Here, we examined the clinical and biological relevance of miR-340 and the molecular pathways regulated by miR-340 in PDAC.MethodsCD47and miR-340 expression and the relationship with cancer patient survival were analyzed by bioinformatics. The mechanism of miR-340 action was explored through bioinformatics, luciferase reporter, qRT-PCR and western blot analyses. The effects of miR-340 on cancer cells were analyzed in terms of apoptosis, proliferation, migration and phagocytosis by macrophages.In vivotumorigenesis was studied in orthotopic and subcutaneous models, and immune cells from the peripheral and tumor immune microenvironments were analyzed by flow cytometry. Depletion of macrophages was used to verify the role of macrophages in impacting the function of miR-340 in tumor progression.ResultsmiR-340 directly regulates and inversely correlates withCD47,and it predicts patient survival in PDAC. The restoration of miR-340 expression in pancreatic cancer cells was sufficient to downregulateCD47and promote phagocytosis of macrophages, further inhibiting tumor growth. The overexpression of miR-340 promoted macrophages to become M1-like phenotype polarized in peripheral and tumor immune microenvironments and increased T cells, especially CD8+T cells, contributing to the antitumor effect of miR-340.ConclusionsmiR-340 is a key regulator of phagocytosis and antitumor immunity, and it could offer a new opportunity for immunotherapy for PDAC.

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