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J Cell Physiol. 2019 Sep 5. doi: 10.1002/jcp.29128. [Epub ahead of print]

Decreasing New York esophageal squamous cell carcinoma 1 expression inhibits multiple myeloma growth and osteolytic lesions.

Author information

1
Department of Pathogenic Biology and Immunology, School of Medicine, Southeast University, Nanjing, China.
2
Changzhou Blood Center, Changzhou, China.
3
Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
4
Department of Oncology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.

Abstract

New York esophageal squamous cell carcinoma 1 (NY-ESO-1) is aberrantly expressed in multiple myeloma (MM) patients, however, its role remains largely unknown. The present study aimed to investigate the effect of NY-ESO-1 knockdown on MM impact and provide evidence for targeting treatment of MM. Human MM U266 cells were infected with lentivirus-based small hairpin RNA-targeting NY-ESO-1 (LV-shNY-ESO-1). Cellular proliferation, colony-forming, migration, and invasion assays were employed. The expressions of cell cycle and epithelial-mesenchymal transition (EMT)-related molecules, MM growth, and mouse osteolytic lesions were evaluated. The results showed that the LV-shNY-ESO-1-U266 cells had a lower expression of NY-ESO-1 and a higher expressions of p21 and E-cadherin, and a weaker abilities of colony formation, drug-resistant to adriamycin, migration, and invasion than those of the control cells. Importantly, the knockdown of NY-ESO-1 inhibited significantly the U266 cell-induced MM growth and osteolytic lesions along with increasing the expressions of E-cadherin, p21, and p53 in mice challenged with LV-shNY-ESO-1-U266 cells. Collectively, our findings demonstrate that knockdown of NY-ESO-1 suppressed the U266 cell-induced MM growth and osteolytic lesions by inhibition of the MMs cell cycle and EMT. The NY-ESO-1 knockdown may be considered for future clinical trials in MM.

KEYWORDS:

New York esophageal squamous cell carcinoma 1; RNA interference; epithelial-mesenchymal transition; multiple myeloma; targeted therapy

PMID:
31489631
DOI:
10.1002/jcp.29128

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