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Updated: Aug 28, 2025
06:24
Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
Published on: April 11, 2025
495
Upregulated Apelin Signaling in Pancreatic Cancer Activates Oncogenic Signaling Pathways to Promote Tumor Development
Carline Chaves-Almagro1, Johanna Auriau1, Alizée Dortignac1
1Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
International Journal of Molecular Sciences
|September 23, 2022
Summary
Apelin signaling promotes pancreatic cancer growth by activating key pathways and increasing cell proliferation and migration. Blocking the apelin receptor (APJ) reduced tumor burden, highlighting apelin as a potential therapeutic target for pancreatic ductal adenocarcinoma (PDAC).
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pancreatic ductal adenocarcinoma (PDAC) remains a significant challenge with limited targeted therapies.
- Understanding the molecular mechanisms driving PDAC progression is crucial for developing new treatments.
Purpose of the Study:
- To investigate the role of the apelin signaling pathway in human pancreatic cancer.
- To determine if apelin and its receptor, APJ, are potential therapeutic targets for PDAC.
Main Methods:
- Immunohistochemistry was used to analyze apelin and APJ expression in human PDAC tissues and mouse models.
- Cell-based assays (Western blot, proliferation, migration, glucose uptake) and orthotopic xenograft experiments characterized apelin signaling in tumor cells.
Main Results:
- Apelin and APJ were co-expressed in invasive PDAC tumor cells.
- Apelin signaling activated PI3K/Akt, upregulated β-catenin, c-myc, and cyclin D1, promoting proliferation, migration, and glucose uptake.
- Blocking the apelin receptor reduced cancer cell proliferation and pancreatic tumor burden.
Conclusions:
- The apelin signaling pathway plays a protumoral role in pancreatic ductal adenocarcinoma.
- Targeting the apelin/APJ pathway represents a promising novel therapeutic strategy for PDAC.
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