SMAD2 and neoplasm: In-vivo experiments showed that JPJD could upregulate the expression of E-cadherin and downregulate the levels of p-Smad2/3 and Snail in orthotopic CRC tumor tissues in nude mice, suggesting that JPJD may inhibit TGF-β-induced EMT via the expression of Snali/E-cadherin mediated by the TGF-β/Smad2/3 signaling pathway, thus exerting anti-CRC invasive and metastatic effects.