Breast cancer cells surrounded by fat cells, illustrating the role of autotaxin in tumor growth.

Breast Cancer's Hidden Allies: How Fat Cells Fuel Tumor Growth

Elliot Brynn in Health & Wellness December 2025 • 4 min read.

"Unveiling the role of fat tissue and its complex relationship with breast cancer progression, offering new targets for therapy."

Breast cancer is a major health concern for women, affecting one in eight during their lifetime. While advancements in detection and treatment have improved outcomes, resistance to therapies remains a significant challenge. Researchers are constantly seeking new targets to disrupt cancer's growth and spread, and one promising area involves understanding the tumor microenvironment – the complex ecosystem surrounding cancer cells.

A key player in this microenvironment is fat tissue, specifically the adipocytes (fat cells) that reside within it. These cells aren't just passive bystanders; they actively interact with cancer cells, influencing their behavior. Recent studies have highlighted the role of autotaxin (ATX), a protein produced by fat cells, in promoting breast cancer progression. ATX leads to the creation of lysophosphatidic acid (LPA) in the body.

New research dives into the specific roles different mammary cell types play in the ATX-LPA axis, aiming to pinpoint the main contributors of ATX within both cancerous and healthy breast tissue. By understanding these cellular interactions, scientists hope to identify more effective therapeutic targets.

Decoding the Fat-Cancer Connection: ATX and LPA

Breast cancer cells surrounded by fat cells, illustrating the role of autotaxin in tumor growth.

The study meticulously isolated and compared various cell populations from breast tumors and healthy mammary tissue. These included:

Epithelial cells (cells that line the mammary ducts)
Mesenchymal cells (cells that provide structural support)
Adipose-derived stem cells (ADSCs) from fat tissue near and far from tumors
Healthy ADSCs

These cells were then analyzed for their expression of LPA receptors (LPARs) and their ability to produce ATX. LPARs are proteins on the cell surface that bind to LPA, triggering various cellular responses.

The results revealed a fascinating division of labor:

ADSCs and mesenchymal cells predominantly expressed LPAR1, while epithelial cells mainly expressed LPAR6.
ADSCs were the primary producers of ATX, particularly those found in tumor-adjacent fat tissue. This production decreased when healthy ADSCs were induced to differentiate into mature fat cells, but increased in ADSCs from tumor patients.
Cancer cell lines themselves did not express ATX.

This highlights the critical role of fat cells in fueling the ATX-LPA axis within the tumor microenvironment.

Targeting the Source: A New Avenue for Treatment

This research underscores the complex interplay between cancer cells and their surrounding environment. By identifying ADSCs and adipocytes as the main producers of ATX in breast cancer, the study points to a potential new therapeutic strategy: targeting the ATX-LPA axis.

The study also found that each mammary cell population plays a different role in the ATX-LPA axis with ADSCs and adipocytes being the main source of ATX in tumor patients in our experimental setting. Inhibitors of this axis may therefore present a valuable target for pharmacological therapies.

Inhibiting ATX could disrupt the LPA production, potentially starving the tumor and reducing its ability to grow and spread. Further research is needed to explore the effectiveness and safety of ATX inhibitors in breast cancer treatment, but this study provides a strong rationale for pursuing this approach. It also opens avenues for personalized medicine, where treatments are tailored based on the specific characteristics of a patient's tumor microenvironment.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1186/s12885-018-5166-z, Alternate LINK

Title: Adscs And Adipocytes Are The Main Producers In The Autotaxin–Lysophosphatidic Acid Axis Of Breast Cancer And Healthy Mammary Tissue In Vitro

Subject: Cancer Research

Journal: BMC Cancer

Publisher: Springer Science and Business Media LLC

Authors: Rafael Schmid, Katharina Wolf, Jan W. Robering, Selina Strauß, Pamela L. Strissel, Reiner Strick, Matthias Rübner, Peter A. Fasching, Raymund E. Horch, Andreas E. Kremer, Anja M. Boos, Annika Weigand

Published: 2018-12-01

Everything You Need To Know

What is Autotaxin (ATX), and what role does it play in breast cancer?

Autotaxin, or ATX, is a protein produced primarily by fat cells, specifically adipocytes, within the breast tumor microenvironment. Its main function is to produce lysophosphatidic acid, or LPA, which then interacts with various cell types to influence cancer progression. Cancer cells themselves do not express ATX. The fat cells near the tumors are the primary source.

How could targeting the ATX-LPA axis potentially lead to new treatments for breast cancer?

Targeting the ATX-LPA axis could disrupt the communication between fat cells and cancer cells. Since fat cells, particularly ADSCs, are the main producers of ATX, inhibiting ATX production or blocking LPA receptors could potentially slow down or stop tumor growth. This approach is especially promising because cancer cells themselves do not produce ATX, making the tumor microenvironment a key therapeutic target.

Which cell types express LPAR1 and LPAR6, and what is the significance of this difference?

Adipose-derived stem cells, or ADSCs, and mesenchymal cells predominantly express LPAR1, a type of LPA receptor. Epithelial cells, on the other hand, mainly express LPAR6. This difference in receptor expression suggests that different cell types respond differently to LPA, influencing their behavior and contribution to the tumor microenvironment. Understanding these specific interactions can help in developing targeted therapies.

What specific cell populations were compared in the study to understand the fat-cancer connection?

The study compared several types of mammary cells, including epithelial cells (lining mammary ducts), mesenchymal cells (providing structural support), adipose-derived stem cells (ADSCs) from fat tissue near and far from tumors, and healthy ADSCs. By isolating and analyzing these cells, researchers determined the expression of LPA receptors and the ability to produce Autotaxin (ATX).

How does Autotaxin (ATX) production differ between healthy fat cells and fat cells near breast tumors?

The research found that Adipose-derived stem cells, or ADSCs, located near breast tumors produce more Autotaxin, or ATX, than healthy ADSCs. When healthy ADSCs differentiate into mature fat cells, ATX production decreases, but in ADSCs from tumor patients, ATX production increases. These findings indicate that the tumor environment influences fat cells to promote cancer progression via the ATX-LPA axis, making these cells potential therapeutic targets.