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Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells
Published on: May 9, 2020
RYK silencing-modified bone marrow-derived mesenchymal stem cells suppress gastric cancer progression
Yongan Fu1, Zongda Cai1, Yangqiang Wang1
1Department of Gastrointestinal Surgery, Quanzhou First Affiliated Hospital to Fujian Medical University, 250 East Street, Quanzhou, Fujian, 362000, P.R. China.
Abstract:
Gastric cancer (GC) is a prevalent malignant tumor threatening human health. This study aimed to explore the potential mechanism of receptor-like tyrosine kinase (RYK) silencing-modified bone marrow-derived mesenchymal stem cells (BMSCs) in the progression of GC. BMSCs were transfected with the RYK siRNA and negative controls. Cell co-culture experiments were used to explore the interaction between different BMSCs and human gastric carcinoma cell line NCI-N87. Cancer cell proliferation, cell cycle, apoptosis, colony formative ability, and invasive ability were assessed. Western blot analysis was performed to determine the protein levels of cyclinA, Bcl-xL, Bcl-2, cleaved caspase 3, cleaved caspase 7, cleaved caspase 9, and cleaved PARP1 in NCI-N87 cells. Compared with NCI-N87 cells, co-culture of si-NC-modified BMSCs with NCI-N87 cells promoted the proliferation, colony formative ability, and invasion of NCI-N87 cells, inhibited the apoptosis of NCI-N87 cells, and reduced the proportion of NCI-N87 cells present in G2/M phase cells. In addition, compared with the si-NC-BMSCs + N87 group, the si-RYK-BMSCs + N87 group inhibited the proliferation, colony formative ability, and invasion of NCI-N87 cells, promoted the apoptosis of NCI-N87 cells, and increased the proportion of G2/M phase cells. Thus, RYK silencing-modified BMSCs can inhibit the proliferation, colony formative ability, and invasion of NCI-N87 cells, while inducing apoptosis and G2/M phase arrest.
Insights
Silencing receptor-like tyrosine kinase (RYK) in bone marrow-derived mesenchymal stem cells (BMSCs) inhibits gastric cancer (GC) progression. Modified BMSCs reduced cancer cell proliferation and invasion while promoting apoptosis.
Area of Science:
- Oncology
- Cell Biology
- Stem Cell Therapy
Background:
- Gastric cancer (GC) remains a significant global health challenge.
- Bone marrow-derived mesenchymal stem cells (BMSCs) have potential therapeutic applications.
- Understanding the interaction between BMSCs and GC cells is crucial for developing novel treatments.
Purpose of the Study:
- To investigate the mechanism by which receptor-like tyrosine kinase (RYK) silencing in BMSCs affects gastric cancer progression.
- To evaluate the impact of RYK-silenced BMSCs on human gastric carcinoma cell line NCI-87.
Main Methods:
- BMSCs were transfected with RYK siRNA or negative control siRNA.
- Co-culture experiments were performed between modified BMSCs and NCI-87 cells.
- Cell proliferation, cell cycle, apoptosis, colony formation, and invasion assays were conducted.
- Western blot analysis assessed key protein levels related to cell cycle and apoptosis.
Main Results:
- Co-culture with control BMSCs promoted NCI-87 cell proliferation, invasion, and colony formation, while inhibiting apoptosis and G2/M phase arrest.
- RYK-silenced BMSCs significantly inhibited NCI-87 cell proliferation, invasion, and colony formation.
- RYK-silenced BMSCs promoted NCI-87 cell apoptosis and induced G2/M phase arrest.
Conclusions:
- RYK silencing in BMSCs demonstrates anti-cancer properties against gastric cancer cells.
- RYK-silenced BMSCs can serve as a potential therapeutic strategy to inhibit GC progression.
- This study elucidates a novel mechanism involving RYK-modified BMSCs in modulating GC cell behavior.
