Research Paper Volume 16, Issue 2 pp 1620—1639

PROX1 interaction with α-SMA-rich cancer-associated fibroblasts facilitates colorectal cancer progression and correlates with poor clinical outcomes and therapeutic resistance


Figure 7. PROX1 knockdown inhibits xenograft tumor growth in nude mice. PROX1 knockdown reduced HCT116 cell-derived xenograft tumor growth in nude mice (n = 5). (A) Statistical comparison of differences in tumor weights and (B) Tumor size between the sh-NC (Control) and PROX1-shRNA#1 group. Growth curve of HCT116 xenograft tumors monitored in the sh-NC and PROX1-shRNA#1 group. (C) Immunohistochemistry analysis of epithelial-mesenchymal transition (EMT) marker expression (magnification, ×400; scale bar, 50 μm) in xenograft tumor tissues in the sh-NC and shRNA-PROX1#1 group. (D) Western blot analysis of PROX1 expression in tumor tissue samples together with other key markers associated with the EMT process and resistance. β-actin is the loading control. The data are presented as the mean ± standard deviation. *P < 0.05 and **P < 0.01 vs. sh-NC.