**Background**
Colorectal cancer (CRC) remains a significant global health challenge characterized by high metastatic potential and the presence of cancer stem cells, which contribute to tumor recurrence and resistance to therapy. Understanding the factors that enhance the stemness and invasive capacity of CRC cells is crucial for developing effective therapeutic interventions. Beyond oncology, the impact of industrial trans fatty acids on metabolic health, including insulin sensitivity and glucose uptake in muscle and adipose tissues, is a subject of intense scientific investigation. In this context, we will introduce a trans fatty acid used in these research areas – Elaidic acid.
**Definition**
Elaidic acid is an orally active trans fatty acid with the molecular formula C18H34O2. It acts as a modulator of the Wnt/ERK1/2 pathway and influences the expression of various myokines and adipokines.
**In Vitro and In Vivo Studies**
According to the Elaidic acid description, this compound exhibits diverse biological effects across different cell types. In vitro studies demonstrate that Elaidic acid (0-35 μM; 24-48 h) promotes the growth and invasive ability of CT26 and HT29 colorectal cancer cells while reducing their apoptosis in a dose-dependent manner. Furthermore, treatment with 35 μM Elaidic acid for one week enhances the sphere-forming capacity of CT26 cells under hypoxic conditions and concurrent treatment. This process is associated with the upregulation of stem cell markers (nucleostemin, CD133, Oct4) and the dedifferentiation marker c-Myc, alongside the downregulation of differentiation markers such as MUC1, MUC2, and CDX2. Regarding its impact on microbiota, Elaidic acid (0-500 mg/L; 0-24 h) inhibits the growth of several Lactobacillus species, including L. rhamnosus and L. plantarum, and reduces the cell surface hydrophobicity of L. paracasei and L. casei at 200 mg/L. In metabolic models, Elaidic acid (20-500 μM; 24 h) dose-dependently increases TNF-α mRNA levels and decreases IL-15 mRNA levels in differentiated C2C12 myotubes without enhancing insulin-stimulated glucose uptake.
The Elaidic acid in vivo data further support its role in cancer progression. In BALB/c mice, administration of 10 mg/mouse (i.p.) increased the growth of subcutaneous CT26 or HT29 tumors and enhanced peritoneal, liver, and lung metastasis. Additionally, gastric administration (0-0.2 mg/kg; i.g.; every 7 days for 4 weeks) increased the number of CD133-positive cells and metastatic foci in the liver. In conclusion, Elaidic acid is a trans fatty acid that promotes colorectal cancer progression via the Wnt/ERK1/2 pathway and modulates metabolic and microbial environments.
Keywords
Elaidic acid, 112-79-8, Apoptosis, Wnt, ERK, Bacterial, Interleukin Related, Extracellular signal regulated kinases, IL, ERK1/2, HT29 colorectal cancer cells, IL-15, C2C12 myotubes, TNF-α, colorectal cancer, CT26 colorectal cancer cells, insulin resistance, Inhibitor, inhibitor, inhibit
References
[1] Ohmori H, et al. Elaidic Acid, a Trans-Fatty Acid, Enhances the Metastasis of Colorectal Cancer Cells. Pathobiology. 2017;84(3):144-151.
[2] Wu Q, et al. Effects of elaidic acid, a predominant industrial trans fatty acid, on bacterial growth and cell surface hydrophobicity of lactobacilli. J Food Sci. 2014;79(12):M2485-M2490.
[3] Granados N, et al. Distinct effects of oleic acid and its trans-isomer elaidic acid on the expression of myokines and adipokines in cell models. Br J Nutr. 2011;105(8):1226-1234.