1. Annexin A2 combined with TTK accelerates esophageal cancer progression via the Akt/mTOR signaling pathway.
- Author
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Liu R, Lu Y, Li J, Yao W, Wu J, Chen X, Huang L, Nan D, Zhang Y, Chen W, Wang Y, Jia Y, Tang J, Liang X, and Zhang H
- Subjects
- Humans, Animals, Cell Line, Tumor, Mice, Nude, Mice, Esophageal Squamous Cell Carcinoma pathology, Esophageal Squamous Cell Carcinoma metabolism, Esophageal Squamous Cell Carcinoma genetics, Cell Movement, Cell Cycle Proteins metabolism, Cell Cycle Proteins genetics, Male, Mice, Inbred BALB C, Neoplasm Invasiveness, Gene Expression Regulation, Neoplastic, Female, TOR Serine-Threonine Kinases metabolism, Annexin A2 metabolism, Annexin A2 genetics, Proto-Oncogene Proteins c-akt metabolism, Esophageal Neoplasms pathology, Esophageal Neoplasms metabolism, Esophageal Neoplasms genetics, Signal Transduction, Disease Progression, Cell Proliferation, Epithelial-Mesenchymal Transition genetics
- Abstract
Annexin A2 (ANXA2) is a widely reported oncogene. However, the mechanism of ANXA2 in esophageal cancer is not fully understood. In this study, we provided evidence that ANXA2 promotes the progression of esophageal squamous cell carcinoma (ESCC) through the downstream target threonine tyrosine kinase (TTK). These results are consistent with the up-regulation of ANXA2 and TTK in ESCC. In vitro experiments by knockdown and overexpression of ANXA2 revealed that ANXA2 promotes the progression of ESCC by enhancing cancer cell proliferation, migration, and invasion. Subsequently, animal models also confirmed the role of ANXA2 in promoting the proliferation and metastasis of ESCC. Mechanistically, the ANXA2/TTK complex activates the Akt/mTOR signaling pathway and accelerates epithelial-mesenchymal transition (EMT), thereby promoting the invasion and metastasis of ESCC. Furthermore, we identified that TTK overexpression can reverse the inhibition of ESCC invasion after ANXA2 knockdown. Overall, these data indicate that the combination of ANXA2 and TTK regulates the activation of the Akt/mTOR pathway and accelerates the progression of ESCC. Therefore, the ANXA2/TTK/Akt/mTOR axis is a potential therapeutic target for ESCC., (© 2024. The Author(s).)
- Published
- 2024
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