ArticleArchives of endocrinology and metabolism2025
MAP17 contributes to the tumorigenesis of papillary thyroid carcinoma by activating the AKT signaling pathway.
Article in Archives of endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
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Authors and funding
4 authors.
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Abstract
objectiveThis 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
methodsWe 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.
resultsCell 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.
conclusionOur 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.
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