Int J Biol Sci 2019; 15(7):1419-1428. doi:10.7150/ijbs.34076
TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT
1. Jiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address)
2. School Of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China
3. Key Laboratory Of Environmental Medicine Engineering, Ministry Of Education And School Of Public Health, Southeast University, Nanjing, Jiangsu, China
#Both authors contributed equally to this work
Objectives: keratin 16 (KRT16) is a type I cytokeratin that overexpressed in many kinds of cancers, but unlike other keratins, KRT16 was poorly studied, so the aim of current study was to determine the biological role of KRT16 in lung adenocarcinoma (LUAD).
Materials and Methods: by utilizing open access data, we determined KRT16 expression in LUAD. After that we evaluated the biological role of KRT16 in-vitro and in-vivo. We also explored the reason for KRT16 overexpression. Last, we explored the clinical significance of KRT16 in LUAD.
Results: we found KRT16 is overexpressed in LUAD and positively correlated with lymph node metastasis. Knockdown of KRT16 significantly influenced the LUAD cells' migration, invasion, proliferation and epithelial-mesenchymal transition (EMT). Moreover, TFAP2A could transcriptionally overexpress KRT16, which contributed to the TFAP2A tumorigenicity. Last, we determined that high level of KRT16 predicts poor prognosis of LUAD patients.
Conclusions: our data indicate that, TFAP2A induced KRT16 overexpression promotes tumorigenicity in LUAD via EMT, and KRT16 expression could serve as an independent prognosis marker.
Keywords: TFAP2A, KRT16, LUAD, EMT, Keratin
Yuanhua L, Pudong Q, Wei Z, Yuan W, Delin L, Yan Z, Geyu L, Bo S. TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT. Int J Biol Sci 2019; 15(7):1419-1428. doi:10.7150/ijbs.34076. Available from http://www.ijbs.com/v15p1419.htm