Abstract
A mouse gastric cancer model is an important tool for studying the mechanisms of gastric cancer. To establish subcutaneously implanted tumors, MKN-45 cell suspensions and tumor tissues were implanted into the middle of the right armpit of nude mice. To generate an abdominal metastasis model, MKN-45 cell suspensions and tumor tissue homogenates were implanted into the middle of the lower abdomen. We measured the weights of the nude mice and the longest dimension, shortest dimension, thickness, and volume of the tumor. We also analyzed the rate of tumor formation, the time required for tumor formation, and the number and size of abdominal tumors in the mice. The rates of formation of the subcutaneously implanted tumors were 100%, 0%, and 100% in the nude mice inoculated with 2 × 107 cells/mL or 1 × 107 cells/mL of the MKN-45 cell suspension or the tumor tissue homogenate (2 × 107 cells/mL), respectively. The rates of metastatic abdominal tumor formation were 100%, 50%, and 75% in mice inoculated with 5 × 107 cells/mL or 1 × 107 cells/mL of the tumor tissue homogenate or the MKN-45 cell suspension (5 × 107 cells/mL), respectively. We derived tumor tissues and tumor tissue homogenates from nude mice prior to establishing the subcutaneous model of implanted tumors and the abdominal metastasis model of gastric cancer, respectively.
Highlights
Gastric cancer (GC) is the fourth most common cancer and the third most common cancer-related cause of death worldwide [1]
Tumors were observed in nude mice (4/4, 100%) subcutaneously inoculated with the more concentrated MKN-45 cell suspension (200 μL, 2 × 107 cells/mL)
The tumor formation rate was 100% (4/4) in the nude mice inoculated with the tumor tissue homogenate
Summary
Gastric cancer (GC) is the fourth most common cancer and the third most common cancer-related cause of death worldwide [1]. GC patients have low rates of radical resection surgery and short overall survival time (the median overall survival duration is less than 1 year) [5]. Molecular therapies that target a variety of mechanisms may be developed into efficient methods to treat GC. These targeted mechanisms include the regulation of epidermal growth factor, angiogenesis, immune checkpoint blockades, the cell cycle, cell apoptosis, key enzyme levels and c-Met, mTOR, and insulin-like growth factor receptor signaling [6,7,8]
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