Abstract

 
 
 
 Purpose: To investigate the role of pancreatic adenocarcinoma up-regulated factor (PAUF) in lung cancer.
 Method: Proliferation of lung cancer cell lines (A549 and H1299) was determined using MTS and Edu staining assays. Wound healing and transwell assays were performed to evaluate cell migration and invasion abilities. Lung cancer stem cell (CSC) marker expressions, including CD133, CD44, ALDH1, SOX2, and Oct4, were determined by western blot assay.
 Results: Knockdown of PAUF significantly inhibited A459 and H1299 cell proliferation (p < 0.01). The wound healing and transwell assay results indicated that depletion of PAUF markedly suppressed H1299 and A549 cell migration and invasion, compared with the control cells (p < 0.01). Knockdown of PAUF reduced distinct CSC marker expression, suggesting inhibition of CSC phenotypes, and reduced phosphorylated focal adhesion kinase (FAK), phosphorylated Src, and phosphorylated extracellular signal-regulated kinase (ERK), but not total FAK, Src, and ERK. These results suggested that knockdown of PAUF deactivated the FAK/Src/ERK signal pathway.
 Conclusion: Knockdown of PAUF inhibits lung cancer cell proliferation, migration, invasion, and CSC properties via deactivation of FAK/Src/ERK signal pathway. These results may provide a novel strategy for the development of lung cancer therapeutics.
 
 
 
Highlights
Lung cancer is a malignant tumor and causes high incidence and mortality rates worldwide [1]
The MTS assay results indicated that knockdown of Pancreatic adenocarcinoma up-regulated factor (PAUF) suppressed cell viability of the H1299 and A549 cells (Figure 1 C)
These findings indicated that knockdown of PAUF inhibited H1299 and A549 cell proliferation
Summary
Lung cancer is a malignant tumor and causes high incidence and mortality rates worldwide [1]. Expression of PAUF is closely associated with a poor prognosis for cervical cancer patients [9]. It has been found to be an endogenous ligand for toll-like receptor 4, leading to activation of JNK, AKT and ERK signaling in human leukemia cells [8,12] Given these findings, it has been hypothesized that PAUF might participate in lung cancer. Virus was resuspended, added to a 6-well plate, and cultured with H1299 and A549 cells for 72 hours. After a 24-hour cell culture, each well was added with EdU solution for 2-h incubated at 37 °C. Approximately 2 × 103 cells/well H1299 and A549 cells were seeded in 6-well plates (Corning, New York, USA).
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