CD146 promotes migration and proliferation in pulmonary large cell neuroendocrine carcinoma cell lines

  • Oncol Lett. 2019 Feb;17(2):2075-2080. doi: 10.3892/ol.2018.9830.
Yicui Piao  1 ,  Hongyu Guo  2 ,  Zhibo Qu  3 ,  Biao Zheng  4 ,  Yong Gao  1  5
Affiliations
  • 1. Department of Critical Care Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong 518116, P.R. China.
  • 2. Department of Medical Administration, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
  • 3. Department of General Surgery, Harbin Children Hospital, Harbin, Heilongjiang 150001, P.R. China.
  • 4. Department of Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong 518116, P.R. China.
  • 5. Department of Critical Care Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, P.R. China.
PMID: 30675274 DOI: 10.3892/ol.2018.9830
Abstract

Dysregulated expression of the cell surface protein, CD146, has been implicated in various types of Cancer in humans, including in Lung Cancer. The present study aimed to clarify the mechanism underlying abnormal CD146 expression in human pulmonary large cell neuroendocrine carcinoma (LCNEC) cell lines (NCI-H460 and NCI-H810). The functions of CD146 were investigated by measuring cell migration and viability following CD146 knockdown or overexpression via small interference RNA and plasmid transfection. The findings demonstrated that decreased protein expression of CD146 could inhibit migration and viability in LCNEC cells. Furthermore, CD146 was determined to influence the expression of epithelial-mesenchymal transition markers (epithelial Cadherin, vimentin and Snail) and promoted Akt phosphorylation. The present results imply CD146 may function in the migration and proliferation of pulmonary LCNEC cells.

Keywords
AKT; cluster of differentiation 146; epithelial-mesenchymal transition; pulmonary large cell neuroendocrine carcinoma.