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Updated: Jan 10, 2026

Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
Published on: March 31, 2016
Fatty acids modulate the colorectal cancer immune microenvironment via regulating the interaction and transactivation
Binyan Xu1, Xufeng Hou2, Maoyuan Wang1
1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract:
Dietary fatty acids accelerate cancer development and metastasis by altering the tumor microenvironment (TME), yet the mechanism is unclear. Here, two-sample Mendelian randomization (MR) revealed that BMI impairs colorectal cancer (CRC) immune surveillance. Additionally, a high-fat diet (HFD) reshapes the immunosuppressive TME, hallmarked by increased myeloid-derived suppressor cells and decreased CD8+ T cells in mice. Mechanistically, the unhealthy fatty acid palmitic acid (PA) binds to its nuclear receptors, peroxisome proliferator-activated receptors (PPARs), enhancing PPARδ while inhibiting PPARα and P53 transactivation, thereby upregulating CD73 and downregulating tumor necrosis factor-related apoptosis-inducing ligand receptors 1 and 2 (TRAIL-R1/2), which drives immunosuppression in CRC transplant tumors. Conversely, conjugated linoleic acid (CLA), a healthy fatty acid, enhances PPARα and P53 transactivation while inhibiting PPARδ transactivation, leading to decreased CD73 and increased TRAIL-R1/2, which enhances anti-tumor immunity and limits metastasis. These findings suggest a direct, universal mechanism by which fatty acid composition regulates immune homeostasis and tumor progression via PPARα/δ-P53 crosstalk.
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