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Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
Published on: November 28, 2019
Immunomodulation via macrophages to fight solid tumor malignancies
Hiren Dandia1, Prakriti Tayalia1
1Department of Biosciences and Bioengineering, Indian Institute of Technology Bombay, India.
Abstract:
The paper 'A C-Terminal Fragment of Adhesion Protein Fibulin-7 Inhibits Growth of Murine Breast Tumor by Regulating Macrophage Reprogramming' by Chakraborty et al. highlights that Fbln7-C could be explored as a potential immunomodulatory agent against various solid cancers and have shown its abilities to regulate tumor microenvironment reprogramming of TAMs in a breast cancer model. Fbln7, which is a secreted glycoprotein, has been shown to be anti-angiogenic and has an immunomodulatory role regulating various functional properties of monocytes, macrophages, and neutrophils, thereby influencing inflammation. In this study, the authors have shown that in a murine breast tumor model, intravenous administration of Fbln7-C significantly reduces the size of tumors via macrophage reprogramming. Comment on: https://doi.org/10.1111/febs.15333.
Insights
A Fibulin-7 fragment (Fbln7-C) shows potential as an immunomodulatory agent. It effectively reduced murine breast tumor size by reprogramming tumor-associated macrophages (TAMs).
Area of Science:
- Immunology
- Oncology
- Biochemistry
Background:
- Fibulin-7 (Fbln7) is a secreted glycoprotein with known anti-angiogenic and immunomodulatory roles.
- Fbln7 influences the function of immune cells like monocytes and macrophages, impacting inflammation.
- Tumor-associated macrophages (TAMs) play a critical role in regulating the tumor microenvironment.
Purpose of the Study:
- To investigate the therapeutic potential of a C-terminal fragment of Fibulin-7 (Fbln7-C) in a murine breast cancer model.
- To determine if Fbln7-C can modulate the tumor microenvironment by reprogramming TAMs.
Main Methods:
- Intravenous administration of Fbln7-C in a murine breast tumor model.
- Assessment of tumor size reduction and analysis of macrophage reprogramming.
Main Results:
- Intravenous Fbln7-C administration significantly reduced murine breast tumor size.
- Fbln7-C demonstrated the ability to reprogram TAMs within the tumor microenvironment.
Conclusions:
- The C-terminal fragment of Fibulin-7 (Fbln7-C) is a promising immunomodulatory agent for cancer therapy.
- Fbln7-C's efficacy in reducing tumor growth is linked to its ability to reprogram TAMs, highlighting its potential against solid cancers.
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