Copyright: ©Author(s) 2026.
World J Gastroenterol. Mar 21, 2026; 32(11): 113325
Published online Mar 21, 2026. doi: 10.3748/wjg.v32.i11.113325
Published online Mar 21, 2026. doi: 10.3748/wjg.v32.i11.113325
Figure 6 Icariin represses epithelial-mesenchymal transition in colorectal cancer cells as well as recruitment of C-X-C motif chemokine receptor 2+ tumor-associated neutrophils, and promotes immune activation by up-regulating SMAD4 expression.
A: The relative expression of protein E-cadherin, α-catenin, and vimentin; B: The proportion of C-X-C motif chemokine receptor 2+ tumor-associated neutrophils in the lower chamber. Results are illustrated as mean ± SD. aP < 0.05 vs the small interfering SMAD4-negative control group, bP < 0.05 vs the small interfering SMAD4 group, cP < 0.05 vs the icariin + small interfering-negative control group. ICA: Icariin; siSMAD4: Small interfering SMAD4; NC: Negative control; GAPDH: Glyceraldehyde 3-phosphate de hydrogenase; CXCR2: C-X-C motif chemokine receptor 2.
- Citation: Zhao YH, Chen J, Gong T, Ge HY, Li M. Icariin inhibits tumor-associated neutrophil recruitment via the CXCL8-CXCR2 axis and restrains pro-metastatic programs in colorectal cancer. World J Gastroenterol 2026; 32(11): 113325
- URL: https://www.wjgnet.com/1007-9327/full/v32/i11/113325.htm
- DOI: https://dx.doi.org/10.3748/wjg.v32.i11.113325