Macrophage-Organoid Coculture Model Development Service

Creative Biolabs offers a specialized model development service that explores the intricate crosstalk between macrophages and cancer cells, particularly in enabling cancer cells to acquire stem-like properties and develop chemoresistance. This service leverages our expertise in cell culture and model construction to bridge the gap in understanding the dynamics between these cells. By establishing a coculture model between cancer organoids and macrophages, we aim to unravel the underlying mechanisms of their interactions and provide invaluable insights for potential clinical applications.

Fig.1 Targeting the macrophage-CCL5-SP1-AREG loop decreases cancer stem-like characteristics and chemoresistance in pancreatic adenocarcinoma.¹

Macrophage-Organoid Coculture Model Development Service at Creative Biolabs

Creative Biolabs' macrophage-organoid coculture model development service takes advantage of coculturing technologies to mimic the disease microenvironment in vitro, which acts in an essential position in therapeutic strategy development. This innovative method could revolutionize our understanding of disease mechanisms and lead to groundbreaking advancements in personalized treatments. By utilizing the enzymatic dissociation of diseased tissues into single cells and transwell inserts to separate macrophages and organoids, our service enables the evaluation of compound efficacy through various cellular responses such as cytokine release and cell migration.

Furthermore, our macrophage therapeutic platform includes a set of matured technologies, such as flow cytometry, western blot, etc. Backed up by these advanced technologies and our competent research team, Creative Biolabs is confident in delivering customized macrophage-organoid coculture models with good performance in a shorter turnaround.

Advanced Technologies at Creative Biolabs

ELISA	Sphere Formation Analysis
Flow Cytometry	Single-cell RNA-sequencing analysis
Western Blotting	Gene Expression Omnibus (GEO) analysis
Immunofluorescence	Cytokine Microarray Analysis

Published Data

Background:	Gemcitabine resistance (GR) in pancreatic adenocarcinoma is influenced by interactions with macrophages in the tumor microenvironment. Investigating this relationship could lead to the discovery of innovative treatment strategies for addressing GR in pancreatic adenocarcinoma.
Method:	Research is conducted to assess the impact of macrophage stimulation on gemcitabine resistance in pancreatic adenocarcinoma. Co-cultures involving patient-derived organoids (PDOs) from three PAAD cases and macrophages were implemented. Through analyzing data from various sources, including cytokine arrays, genomic databases, and single-cell sequencing data, researchers are able to uncover the signaling factors involved in the crosstalk between macrophages and pancreatic cancer cells, providing valuable insights into gemcitabine resistance mechanisms.
Result:	This study emphasizes the importance of utilizing the PDO model for preclinical research and precision medicine. It reveals a macrophage-CCL5-Sp1-AREG feedback loop that enhances stemness in PCCs, contributing to GR through the activation of the CCR5/AKT/SP1/CD44 pathway. The synergistic effect of gemcitabine and mithramycin presents a promising therapeutic approach for PAAD treatment in various models, including cell lines, PDOs, and mouse studies.

Fig.2 The CCL5/AREG loop allows the communication between macrophages and PCCs. (Jiang, et al., 2023) Fig.2 The CCL5/AREG loop enables communication between macrophages and PCCs.¹

Key Advantages

Ph.D. research team.
Robust technology platform.
Strict quality control.
Customized service.
Standard reports delivery.

For more details about our macrophage-organoid coculture model development service, please don't hesitate to reach out to us.

Reference

Jiang, Shengwei, et al. "Macrophage-organoid co-culture model for identifying treatment strategies against macrophage-related gemcitabine resistance." Journal of Experimental & Clinical Cancer Research 42.1 (2023): 199.