What question did this study set out to answer?

This research aims to explore the role of ADGRF1 in promoting pancreatic ductal adenocarcinoma (PDAC) progression and identify its biological implications.

March 16, 2026Open Access

Adhesion G protein-coupled receptor ADGRF1 promotes pancreatic ductal adenocarcinoma progression by modulating YY1/CTSD signaling axis

Key Result

High expression of ADGRF1 in pancreatic ductal adenocarcinoma was significantly correlated with poor patient prognosis and promoted malignant phenotypes in PDAC cells.

Key Points

This research aims to explore the role of ADGRF1 in promoting pancreatic ductal adenocarcinoma (PDAC) progression and identify its biological implications.
Conducted bioinformatics analysis of ADGRF1 expression in PDAC tissues
Performed in vivo experiments to assess tumor progression with ADGRF1 deletion
Examined the modulation of YY1 and CTSD in PDAC cells
Analyzed mTOR signaling pathway activation in relation to ADGRF1 activity
ADGRF1 shows abnormal expression in PDAC tissues, correlating negatively with patient prognosis
High ADGRF1 expression is linked to increased tumor phenotypes like proliferation and migration
Deletion of ADGRF1 significantly inhibits tumor progression in vivo
ADGRF1 regulates YY1 expression, which activates CTSD and upregulates the mTOR signaling pathway

Structured PICO

Population

Pancreatic ductal adenocarcinoma (PDAC) tissues, PDAC cells, and in vivo models

Intervention

Deletion or modulation of ADGRF1

Comparator

Control/wild-type

Outcome

Tumor progression and malignant phenotypes (proliferation, stemness, migration, and invasion)surrogate

ADGRF1 promotes pancreatic ductal adenocarcinoma progression via the YY1/CTSD/mTOR axis, highlighting it as a potential therapeutic target.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a 5-year survival rate of merely 10%, underscoring the urgent need for new therapeutic targets. In this study, we investigated the driving roles of adhesion G-protein coupled receptor F1 (ADGRF1) in PDAC progression and its biological relevance. By bioinformatics analysis, we found that ADGRF1 was abnormally expressed in PDAC tissues, and high expression of ADGRF1 was significantly negatively correlated with patient prognosis. We further determined that ADGRF1 promotes malignant phenotypes such as proliferation, stemness, migration and invasion of PDAC cells. And in vivo experiments have shown that deletion of ADGRF1 inhibit the tumor progression of PDAC. We demonstrated the molecular mechanism that ADGRF1 regulates the expression of Yin-Yang 1 (YY1) to promote the transcriptional activation of Cathepsin D (CTSD), and thereby upregulates of the mTOR signaling pathway. Taken together, our results describe the promoting effect of ADGRF1 on PDAC progression and may serve as a potential therapeutic target for PDAC.