MAP17 contributes to the tumorigenesis of papillary thyroid carcinoma by activating the AKT signaling pathway.

Abstract

Objective: This study investigates the role of membrane-associated protein 17 (MAP17) and the Akt signaling pathway in the progression of papillary thyroid carcinoma (PTC).

Materials and methods: We conducted a series of in vitro experiments using PTC cell lines (HTori-3 and TPC-1). Cells were divided into three groups: control, MAP17 inhibitor negative control (NC), and MAP17 inhibitor treatment. Cell viability was assessed at 0, 24, 48, and 72 hours using the Cell Counting Kit-8 (CCK-8) assay. Apoptosis levels were measured by flow cytometry, and protein and mRNA expression of MAP17, phosphorylated Akt (p-AKT), and Akt were analyzed by Western blot and qRT-PCR.

Results: Cell viability in the control, MAP17 inhibitor NC, and MAP17 inhibitor groups increased significantly over time (P < 0.05). Notably, in both HTori-3 and TPC-1 cells, the MAP17 inhibitor significantly reduced cell viability compared to the control and NC groups at 24, 48, and 72 hours (P < 0.05). Furthermore, apoptosis levels were significantly higher in the MAP17 inhibitor group compared to the control and NC groups (P < 0.05). Western blot and qRT-PCR analyses revealed that MAP17 and p-Akt protein and mRNA levels were significantly higher in the control and NC groups compared to the MAP17 inhibitor group (P < 0.05). However, no significant differences in total Akt protein or mRNA levels were observed across groups.

Conclusion: Our findings suggest that MAP17 and the Akt signaling pathway play a crucial role in promoting the progression of PTC. Inhibition of MAP17 suppresses cell viability and induces apoptosis, indicating that MAP17 may be a promising therapeutic target for PTC. The data also highlight the potential for targeting the MAP17-Akt axis in developing future treatments for PTC.