Panoply™ Human FLT1 Over-expressing Stable Cell Line

Identifying new therapeutic targets for radioactive iodine-resistant differentiated thyroid cancer (DTC) patients may help improve the prognosis of I131-resistant DTC patients. Here, researchers explored the potential molecular mechanisms of FLT-1 in DTC. The study showed that FLT1 expression was elevated in thyroid cancer cells that had not received I131 treatment. BHT101 cells overexpressing FLT1 exhibited significantly enhanced proliferation, colony formation, migration, and invasion capabilities. Protein expression of TGFβ1 and p-Smad3 was significantly increased in thyroid cancer cells overexpressing FLT1, while SMAD3 expression showed no significant change. Upregulation of FLT1 led to decreased NIS expression. FOXP3, TGF-βR1, and p-Smad3 were co-localized in FLT1-overexpressing BHT101 cells. In vivo experiments showed that tumor volume and tumor weight increased with increasing FLT1 expression. These results suggest that upregulation of FLT1 can activate the TGF-β1/Smad3 pathway, downregulate NIS expression, and enhance the function of thyroid cancer cells.

Here, researchers investigated the apoptosis, proliferation, migration, invasion, and clonogenic ability of cancer cells after FLT1 upregulation. Both CCK-8 and cell cloning assays showed a significant increase in the proliferation rate of BHT101 cells after FLT1 upregulation (Figure 1A-D). After 24 hours of culture, the wound healing distance of FLT1-overexpressing BHT101 cells was significantly increased (Figure 1C and E). The invasive ability of FLT1-overexpressing cells was also enhanced (Figure 1F and G). No apoptosis was observed in FLT1-overexpressing BHT101 cells (Figure 1H and I).

Figure 1. FLT1 promoted the growth of BHT101 tumors. (Zhuang J, et al., 2025)