Abstract |
Lung cancer is one of the most common causes of cancer-related mortality worldwide, which is partially due to its metastasis. However, the mechanism underlying its metastasis remains elusive. In this study, we showed that a low Krüppel-like factor 3 (KLF3) expression level is correlated with a poor prognosis and TNM stages in clinical patients with lung cancer and further demonstrated that KLF3 expression is downregulated in lung cancer tissues compared with adjacent normal samples. In addition, bioinformatics analysis results showed that KLF3 expression is related to lung cancer epithelial-mesenchymal transition (EMT). In vitro and in vivo experiments also showed that KLF3 silencing promotes lung cancer EMT and enhances lung cancer metastasis. More importantly, bioinformatics analysis and in vitro experiments indicated that the role of KLF3 in lung cancer metastasis is dependent on the STAT3 signaling pathway. Overall, our data indicated the crucial function of KLF3 in lung cancer metastasis and suggested opportunities to improve the therapy of patients with lung cancer.
|
Authors | Wei Sun, Shan Hu, Yukun Zu, Yu Deng |
Journal | Molecular carcinogenesis
(Mol Carcinog)
Vol. 58
Issue 11
Pg. 1933-1945
(11 2019)
ISSN: 1098-2744 [Electronic] United States |
PMID | 31486564
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Copyright | © 2019 The Authors. Molecular Carcinogenesis Published by Wiley Periodicals, Inc. |
Chemical References |
- KLF3 protein, human
- Kruppel-Like Transcription Factors
- STAT3 Transcription Factor
- STAT3 protein, human
|
Topics |
- A549 Cells
- Aged
- Animals
- Cell Proliferation
(genetics)
- Computational Biology
- Epithelial-Mesenchymal Transition
(genetics)
- Female
- Gene Expression Regulation, Neoplastic
(genetics)
- Heterografts
- Humans
- Kruppel-Like Transcription Factors
(genetics)
- Lung Neoplasms
(genetics, pathology)
- Male
- Mice
- Middle Aged
- Neoplasm Metastasis
- STAT3 Transcription Factor
(genetics)
|