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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

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CLCA1 Modulates Pancreatic Cancer Proliferation via SIRT1-HIF-1α Pathway.

Dingyuan Hu, Yilei Yang, Jinlin Ge

Clinical Laboratory

|June 15, 2026

Summary

This summary is machine-generated.

Calcium-activated chloride channel regulator 1 (CLCA1) suppresses pancreatic cancer growth by downregulating SIRT1 and HIF-1α. CLCA1 enhances gemcitabine sensitivity, offering a potential therapeutic target for pancreatic ductal adenocarcinoma (PDAC).

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Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies

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Published on: July 3, 2025

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor prognosis and high chemoresistance.
Low calcium-activated chloride channel regulator 1 (CLCA1) expression correlates with worse survival in PDAC patients.
The functional role of CLCA1 in PDAC remains unclear.

Purpose of the Study:

To investigate the function of CLCA1 in pancreatic cancer cells.
To elucidate the molecular mechanisms underlying CLCA1's role in PDAC.
To explore CLCA1 as a potential therapeutic target for PDAC.

Main Methods:

Overexpression of CLCA1 in PANC-1 cells.
Assays for cell proliferation (CCK-8) and invasion (Transwell).
Proteomic analysis (LC-MS/MS) and mechanistic studies (RNA interference, qPCR, Western blotting) of the SIRT1/HIF-1α pathway.

Main Results:

CLCA1 overexpression inhibited PANC-1 cell proliferation and invasion.
CLCA1 enhanced sensitivity to gemcitabine and modulated the SIRT1/HIF-1α axis.
CLCA1 downregulated SIRT1, reducing HIF-1α stabilization and downstream gene expression (GLUT1, LDHA).

Conclusions:

CLCA1 suppresses PDAC proliferation and invasion by modulating the SIRT1/HIF-1α pathway.
CLCA1 may enhance gemcitabine sensitivity, suggesting it as a therapeutic target for PDAC.
CLCA1-based therapies hold promise for improving treatment outcomes in PDAC.