David Barneda
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View article: The exit of naive pluripotency contains a metabolism-induced checkpoint for telomere homeostasis
The exit of naive pluripotency contains a metabolism-induced checkpoint for telomere homeostasis Open
During peri-implantation development, the pluripotent tissue of the early embryo undergoes profound cellular and biochemical reprogramming. These transformations are essential for subsequent development, yet how they are coordinated with t…
View article: Table 1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table 1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Pharmacologic targeting of PPARδ modulates metastasis in vivo.
View article: Figure 1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Induction of EMT-like phenotype and metabolic switch in PDAC cells upon starvation. A, Representative images illustrating morphologic changes for PDAC-354 cells in response to treatment for 72 hours with the complex I inhibitor metformin (…
View article: Figure 7 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 7 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Therapeutic targeting of PPARδ impairs invasion in vitro and metastasis in vivo. A, PDAC-215, 354, and 265 cells were pretreated with PPARδ antagonists GSK0660 (10 μmol/L) and GSK3787 (10 μmol/L) and inverse agonist DG172 (2.5 μmol/L) for …
View article: Table S2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Main chemicals used for in vitro and in vivo treatments
View article: Figure S11 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S11 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
PPARD knockdown modifies the expression ratio between MYC and PGC1A
View article: Figure S14 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S14 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Effects of pharmacological modulation of PPAR-δ on invasion and metastasis in vivo, using the highly metastatic PDX CTCA
View article: Figure S8 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S8 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
EMT induction by PPAR-δ agonists, lipidomic changes and inhibition of EMT by downregulation of PPARD
View article: Figure 3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
PPARD expression is linked to metabolic switch and EMT in patients with PDAC. A, Expression levels of PPARD in PDAC tumors (T) vs. surrounding normal tissue (N) included in the TCGA and GTEx projects. B, Patients were dichotomized for PPAR…
View article: Figure S3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Etomoxir or stromal signals alter different metabolic parameters in PDAC cells
View article: Data from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Data from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
The pronounced desmoplastic response in pancreatic ductal adenocarcinoma (PDAC) contributes to the development of a microenvironment depleted of oxygen and nutrients. To survive in this hostile environment, PDAC cells use various adaptive …
View article: Figure 5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
PPARδ controls the balance between OXPHOS and glycolysis, linked to EMT and metastasis. A,In vitro invasion in PDAC-215, 253, and 354 cells stably transduced with inducible lentiviral vectors expressing either a nontargeting short hairpin …
View article: Table S4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Primers for rt-qPCR used in this study
View article: Figure 6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
PPARδ rewires cellular metabolism regulating MYC/PGC1A balance. A, Expression of MYC, PGC1A, and MYC/PGC1A ratio in PDX-354 after mitochondrial energy deprivation during 48 to 72 hours (n = 4–7). B,MYC and PGC1A reporter assay. Promoter ac…
View article: Figure S9 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S9 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Effects of PPARD knockdown in the expression of genes related with the EMT program in different PDAC PDXs
View article: Figure S2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Incubation with a non-toxic dose of etomoxir and macrophage-conditioned medium does not affect CD133 expression or self-renewal of PDAC cells
View article: Figure S1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Different stimuli promoting mitochondrial energy deprivation or coculture with stromal cells the expression of epithelial-to-mesenchymal transition genes in PDAC cells
View article: Table S3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S3 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Plasmids used in this study
View article: Figure S7 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S7 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Expression of the PPAR family members and downstream targets after incubation with etomoxir and MCM
View article: Table S5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Antibodies used in this study
View article: Table S6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Pharmacological targeting of PPAR-δ modulates metastasis in vivo
View article: Figure 2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 2 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Transcriptomic and scRNA-seq analyses identify metabolic switch and EMT induction upon pseudostarvation. Cells were treated for 48 hours with vehicle (Ctrl), MCM, and 20 μmol/L etomoxir (Eto). A, Gene expression profile as assessed by a ca…
View article: Figure S5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S5 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
EMT induction by etomoxir and MCM in bulk transcriptomics
View article: Figure S12 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S12 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
MYC downregulation reverses the prometastatic phenotype induced by etomoxir and MCM
View article: Figure 4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure 4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Activation of PPARδ initiates invasiveness and metastasis. A,PPARD mRNA expression upon 24 to 48 hours of treatment with MCM, etomoxir (Eto), and 5 μmol/L of the PPARδ agonist GW0742. Pooled data of PDAC-215, 253, and 354 cells (n = 4–7). …
View article: Figure S4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S4 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Incubation with etomoxir and MCM induce epithelial-to-mesenchymal transition at the single-cell level
View article: Table S1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Table S1 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Primary PDAC cells used in this study
View article: Figure S6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S6 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Different expression analyses performed for PPARA and PPARG in the TCGA database
View article: Figure S10 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S10 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
The EMT program is related to MYC upregulation and PGC1A downregulation
View article: Figure S13 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer
Figure S13 from PPARδ Orchestrates a Prometastatic Metabolic Response to Microenvironmental Cues in Pancreatic Cancer Open
Effects of MYC inhibition with mycro3 on EMT genes expression and changes induced by PGC1A overexpression at the functional level