A recently published article in Experimental Biology and Medicine (Volume 247, Issue 10, May, 2022) identifies a potentially important personalized therapy for gastric cancer treatment. The study, led by Dr. Guohua Wang in the Institute of Special Environmental Medicine at Nantong University (China), reports that blocking Musashi-1 expression reduces gastric cancer drug tolerance to chemical drugs.

Gastric cancer is a common digestive malignancy and ranks second in cancer-related deaths. Drug resistance accounts for most of the mortality of gastric cancer. Musashi-1 (MSI1) is an RNA-binding protein that is considered a gastric and intestinal stem cell marker and may act as a biomarker and therapeutic target for gastric cancer. An early event in the formation of gastric cancer is the spread of MSI1-positive cells. Therefore, the authors posited that a clear understanding of the role of MSI1 in gastric cancers may lead to more effective therapeutics for treating gastric cancer.

In this study, Dr. Wang and colleagues used immunohistochemistry to show that MSI1 expression in tumour samples was significantly greater than in the adjacent normal tissue. Further, MSI1 levels corresponded with both patient outcomes and the expression of important indicators of cell division; MSI1 inhibition increased the efficacy of chemical drugs used for treating gastric cancer. Their study provides new insight into the possible application of personalized therapy for gastric cancer and may assist in predicting the chemosensitivity of cancer and the development of more effective gene-directed prodrug therapy.

Dr. Wang said, "We investigated the relationship between Musashi-1 (MSI1) expression and the efficacy of chemotherapeutic drugs in gastric cancer to provide data that might support future clinical trials. Using MSI1 upregulation and downregulation in cell systems, we found that MSI1 modulates proliferation, migration, and invasion and thus is likely to play a key part in the development and progression of gastric cancer. Experiments using PDX mouse models showed that MSI1 inhibition reduced the tolerance of gastric cancer to chemical drugs. si-MSI1 combined with chemotherapeutic drugs was effective in reducing tumor sizes MSI1 potentially influences the chemotherapeutic effect through blood vessel epicardial substance (BVES) pathways, which are thought to be involved in cell adhesion and movement. Our study provides a strategy for the development of personalized treatment for gastric cancer patients and offers potential value in predicting chemosensitivity in tumors."

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said, "Wang and colleagues have provided an elegant study, demonstrating that MSI1 reduces the tolerance of gastric cancer to chemical drugs through modulation of the blood vessel epicardial substance (BVES) signaling pathway. These studies should provide the basis for future clinical trials utilizing a combination of drug-si-MSI1 treatment."

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