Purpose: This study focused on the role and mechanism of IGF2BP1 in cell cisplatin resistance of oral squamous cell carcinoma.
Methods: Low-dose intermittent induction method was used to induce cisplatin-sensitive oral squamous cell carcinoma cell line HN30, and establish cisplatin-resistant cell line HN30/DDP. Western blot was used to detect the protein expression level of IGF2BP1 in parental and resistant cell line. Knockdown or overexpression of IGF2BP1 by RNAi and lentivirus transfection method was utilized to analyze the effect of decreased or increased the gene expression of IGF2BP1 on cisplatin resistance. MTT method was used to detect the change of IC50. Statistical analysis of data was performed using SPSS 17.0 software package.
Results: Cisplatin-resistant oral squamous cell carcinoma cell line was successfully established. The IC50 of the drug-resistant cells was significantly higher than that of the parental cells. Knocking down the expression level of IGF2BP1 in drug-resistant strains reduced cell resistance; on the contrary, after overexpression of IGF2BP1 in parental cells dramatically increased cisplatin resistance. Mechanically, activation of Akt signaling pathway was the key factor mediating IGF2BP1 to promote cisplatin resistance in oral squamous cell carcinoma.
Conclusions: IGF2BP1 is significantly associated with cisplatin resistance in oral squamous cell carcinoma. IGF2BP1 can promote cisplatin resistance of oral squamous cells by activating downstream Akt signaling pathway.