β-Catenin and Peroxisome Proliferator-activated Receptor-δ Coordinate Dynamic Chromatin Loops for the Transcription of Vascular Endothelial Growth Factor A Gene in Colon Cancer Cells

Abstract

Background: Mechanism of VEGFA transcription by complex interplay of ␤-catenin and PPAR-␦ remains elusive. Results: The VEGFA promoter was dynamically occupied by ␤-catenin, TCF-4, and PPAR-␦. ␤-Catenin also bound downstream region of the VEGFA gene. Conclusion: ␤-Catenin is responsible for the formation of chromatin loops, which is relieved by PPAR-␦ activation. Significance: Proposed mechanism could provide clues for VEGFA-mediated colon cancer cell initiation.

Role of Wnt Signaling During In-Vitro Bovine Blastocyst Development and Maturation in Synergism with PPARδ Signaling

“…Interestingly, our confocal imaging analysis showed a strong co-localization between β-catenin and PPARδ expression under Wnt stimulated condition (Figure 7). This observation is in agreement with the early findings [19]. It also confirmed the regulation of PPARδ expression by Wnt/β-catenin signaling.…”

“…The stimulation of Wnt activity strongly enhanced the spatial overlapping of PPARδ with β-catenin while PPARδ was randomly overlapped with β-catenin in control group as shown by immune fluorescence analysis ( Figure 7A). This result is consistent with previous study which showed that PPARδ can interact with β-catenin and promote Wnt/β-catenin mediated human colorectal cancer progression [19]. Reversibly, inhibition of PPARδ with Gsk3787 treatment significantly reduced its co-localization with β-catenin.…”

“…Different cancerous and developmental studies reported the cross-talk between Wnt/β-catenin pathway and the nuclear hormone receptor PPARs family [19,43]. PPARδ has been observed to regulate the BL development and implantation process in the mice uterus in response to Cox2 activation [44].…”

Inhibition of Bevacizumab-induced Epithelial–Mesenchymal Transition by BATF2 Overexpression Involves the Suppression of Wnt/β-Catenin Signaling in Glioblastoma Cells

“…To better understand the potential mechanisms for the cause of BV-induced adverse effects, a number of hypotheses were tested, including the observed upregulation of hypoxia-inducible factors (HIFs) related to tumor progression and metastasis (34), particularly in gliomas (13,35). More recently, the importance of the Wnt/β-catenin signaling pathway in EMT regulation has been demonstrated in a variety of tumor types (36)(37)(38). The activation of Wnt/β-catenin signaling was reported to sufficiently induce EMT in glioma cells (39), however, its role in the BV-induced EMT process has not been investigated.…”

An Overview of Gene Regulation by Wnt/β‐Catenin Signaling

“…TCF/β-catenin interactions can antagonize PPARg targets through chromatin loops Jansson et al (2005),Hwang et al (2012)…”