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Updated: Jan 20, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Decreasing New York esophageal squamous cell carcinoma 1 expression inhibits multiple myeloma growth and osteolytic
Fei Li1,2, Fengshu Zhao1, Miao Li1
1Department of Pathogenic Biology and Immunology, 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.
Insights
Knocking down New York esophageal squamous cell carcinoma 1 (NY-ESO-1) in multiple myeloma (MM) cells suppressed tumor growth and bone lesions. This suggests NY-ESO-1 as a potential therapeutic target for MM treatment.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- New York esophageal squamous cell carcinoma 1 (NY-ESO-1) is aberrantly expressed in multiple myeloma (MM), but its function in MM is unclear.
- Understanding NY-ESO-1's role is crucial for developing targeted MM therapies.
Purpose of the Study:
- To investigate the impact of NY-ESO-1 knockdown on multiple myeloma progression.
- To evaluate NY-ESO-1 as a potential therapeutic target for MM.
Main Methods:
- Human MM U266 cells were transduced with lentivirus-expressing short hairpin RNA against NY-ESO-1 (LV-shNY-ESO-1).
- Assays included cellular proliferation, colony formation, migration, invasion, cell cycle, and epithelial-mesenchymal transition (EMT) markers.
- Tumor growth and osteolytic lesions were assessed in vivo in mouse models.
Main Results:
- NY-ESO-1 knockdown reduced MM cell proliferation, colony formation, migration, and invasion.
- LV-shNY-ESO-1 treated cells showed increased expression of p21 and E-cadherin.
- In vivo, NY-ESO-1 knockdown significantly inhibited MM growth and osteolytic lesions, increasing p21, E-cadherin, and p53 expression.
Conclusions:
- NY-ESO-1 knockdown suppresses MM cell cycle and EMT, inhibiting tumor growth and bone destruction.
- Targeting NY-ESO-1 represents a promising strategy for future MM therapeutic interventions.
Related Concept Videos
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10:04Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
08:04Monitoring Tumor Metastases and Osteolytic Lesions with Bioluminescence and Micro CT Imaging
07:02In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
09:41An Organotypic High Throughput System for Characterization of Drug Sensitivity of Primary Multiple Myeloma Cells

