Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Knockdown of pancreatic adenocarcinoma upregulated factor (PAUF) suppresses proliferation, migration, invasion, and cancer stem cell properties in lung cancer cells

Liangchao Dong¹, Weiwei Li², Xiaoli Zhang³

¹Department of Thoracic Surgery; ²Department of Oncology, The First People’s Hospital of Tianmen City, Tianmen City, Hubei Province 431700; ³Department of Pathology, The First Affiliated Hospital of University of South China, Hengyang City, Hunan Province 421001, China.

For correspondence:- Xiaoli Zhang Email: zhangxiaoli6111@126.com Tel:+867348578939

Accepted: 7 March 2021 Published: 31 March 2021

Citation: Dong L, Li W, Zhang X. Knockdown of pancreatic adenocarcinoma upregulated factor (PAUF) suppresses proliferation, migration, invasion, and cancer stem cell properties in lung cancer cells. Trop J Pharm Res 2021; 20(3):459-465 doi: 10.4314/tjpr.v20i3.3

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: PAUF, Proliferation, Migration, Invasion, Cancer stem cell, Lung cancer