Luciferase Reporter Cell Line - HT-22

Suramin, an antitrypanosomal drug, has attracted attention for its potential anticancer activity, partly due to its ability to regulate RNA-binding proteins such as HuR. However, its genome-wide transcriptome effects in oral squamous cell carcinoma remain unclear. Here, researchers performed RNA sequencing on suramin-treated HSC-3 cells and conducted enrichment, network, and transcription factor analyses. In vivo validation was performed in an orthotopic xenograft model using luciferase-labeled HSC-3 cells. Transcriptome analysis revealed widespread downregulation of genes regulating cell cycle progression, chromatin organization, and DNA damage responses, including mitotic regulators such as G2/M phase regulators CCNB1, CDC20, and AURKA, as well as their upstream transcription factors FOXM1 and MYBL2. Conversely, gene expression was upregulated in relation to extracellular matrix remodeling (MMP family and TIMP3) and stress or immune responses (TXNIP and TNFSF10). Functional enrichment analysis confirmed the inhibition of proliferation programs and the activation of tumor-suppressive microenvironment responses. In vivo experiments showed that, compared with the control group, the tumor growth rate in mice treated with suramin was slower, but the difference was not statistically significant. These studies indicate that suramin exerts a dual anti-tumor effect on tongue squamous cell carcinoma by inhibiting proliferative transcriptional programs and regulating extracellular and stress response pathways, laying the foundation for future research to further elucidate its therapeutic significance.

Here, HSC-3-Luc cells (1 × 10⁵) suspended in 30 µl of sterile HBSS were injected orally into the left lingual side of 8-week-old male BALB/cAJcl-nu/nu mice using a 27-gauge needle. Although initially 5 mice were included in each group, due to early accidental deaths, only 4 mice from the vector group and 5 mice from the 20 mg/kg group were ultimately available for longitudinal analysis. Mouse body weight was measured during IVIS imaging and suramin administration. Mice were monitored regularly and euthanized upon reaching a humane endpoint (weight loss >20% and progressive weakness due to tumor burden). Therefore, analysis was limited to day 15, when all mice were alive and the BLI signal was within the linear detection range. Although the BLI value in the 20 mg/kg suramin group was lower than that in the vector group at this point, no significant inter-group effect (P = 0.22) or significant time × inter-group interaction was detected in the mixed-effects model (P = 0.18). The effect size estimates for both the between-group effect (partial η²=0.20) and the time × between-group interaction (partial η²=0.24) were relatively large, but insufficient to determine that suramin had a clear inhibitory effect (Figures 1A and 1B).

Figure 1. In vivo effects of suramin on tumor growth in an orthotopic tongue squamous cell carcinoma model. (Kakuguchi W, et al., 2026)