Ccl26, also known as eotaxin-3, is a member of the eotaxin family. It functions as an eosinophil-selective chemoattractant by interacting exclusively with chemokine receptor 3 (CCR3) [3]. Ccl26 is involved in multiple biological processes such as inflammation and cell migration, and is associated with pathways like the epithelial-mesenchymal transition (EMT) pathway [1].

In a conditional Ccl26 knockout mouse model, depletion of Ccl26 in airway epithelial cells delays the resolution of allergic lung inflammation, indicating that the CCL26-CX3CR1 pathway is pivotal in resolving eosinophilic allergic lung inflammation [2]. In colon cancer cells, Ccl26 siRNAs (a form of loss-of-function) markedly reduced cell viability, proliferation, migration and invasion, accelerated apoptosis, enhanced E-cadherin expression, and reduced N-cadherin and vimentin expression, suggesting that Ccl26 promotes colon cancer progression through regulation of the EMT signaling pathway [1].

In summary, Ccl26 plays a crucial role in inflammation-related processes and cancer progression. The use of gene knockout models, such as the conditional Ccl26 knockout mouse, has been instrumental in revealing its functions in allergic lung inflammation and colon cancer, providing potential therapeutic targets for these diseases.

References:

1. Sun, Aitao, Li, YunHua, Jiang, Xiaodong. 2022. CCL26 silence represses colon cancer by inhibiting the EMT signaling pathway. In Tissue & cell, 79, 101937. doi:10.1016/j.tice.2022.101937. https://pubmed.ncbi.nlm.nih.gov/36156375/

2. Moon, Hyung-Geun, Kim, Seung-Jae, Kim, Ki-Hyun, You, Sungyoung, Park, Gye Young. . CX3CR1+ Macrophage Facilitates the Resolution of Allergic Lung Inflammation via Interacting CCL26. In American journal of respiratory and critical care medicine, 207, 1451-1463. doi:10.1164/rccm.202209-1670OC. https://pubmed.ncbi.nlm.nih.gov/36790376/

3. Shou, Jifei, Peng, Jing, Zhao, Zhikang, Xing, Yanmeng, Liu, Hongbo. 2019. CCL26 and CCR3 are associated with the acute inflammatory response in the CNS in experimental autoimmune encephalomyelitis. In Journal of neuroimmunology, 333, 576967. doi:10.1016/j.jneuroim.2019.576967. https://pubmed.ncbi.nlm.nih.gov/31151084/