TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT

: 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). : by utilizing open access data, we determined KRT16...

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Bibliographic Details
Published in:International journal of biological sciences 2019-01, Vol.15 (7), p.1419-1428
Main Authors: Yuanhua, Liu, Pudong, Qian, Wei, Zhu, Yuan, Wu, Delin, Liu, Yan, Zhang, Geyu, Liang, Bo, Shen
Format: Article
Language:English
Subjects:
Adenocarcinoma
Adenocarcinoma - genetics
Adenocarcinoma - metabolism
Animals
AP-2 protein
Cell Line, Tumor
Cell migration
Cell Movement
Cell Proliferation
Cytokeratin
Epithelial-Mesenchymal Transition
Female
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Humans
Keratin
Keratin-16 - metabolism
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lungs
Lymph nodes
Lymphatic Metastasis
Male
Mesenchyme
Metastases
Mice
Mice, Nude
Middle Aged
Neoplasm Invasiveness
Oncogenes
Prognosis
Research Paper
Tissue Array Analysis
Transcription
Transcription Factor AP-2 - metabolism
Tumorigenicity
Wound Healing
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Summary:: 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). : by utilizing open access data, we determined KRT16 expression in LUAD. After that we evaluated the biological role of KRT16 and . We also explored the reason for KRT16 overexpression. Last, we explored the clinical significance of KRT16 in LUAD. : 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. : our data indicate that, TFAP2A induced KRT16 overexpression promotes tumorigenicity in LUAD via EMT, and KRT16 expression could serve as an independent prognosis marker.
ISSN:1449-2288
1449-2288
DOI:10.7150/ijbs.34076