Abstract
Gastric cancer, one of the most common types of cancers, develops over a series of consecutive histopathological stages. As such, the analysis and research of the gastric precancerous lesions (GPLs) play an important role in preventing the occurrence of gastric cancer. Ginsenoside Rg3 (Rg3), an herbal medicine, plays an important role in the prevention and treatment of various cancers. Studies have demonstrated a correlation between glycolysis and gastric cancer progression. Herein, the aim of the present study was to clarify the potential role for glycolysis pathogenesis in Rg3-treated GPL in Atp4a−/− mice. The GPL mice model showed chronic gastritis, intestinal metaplasia, and more atypical hyperplasia in gastric mucosa. According to the results of HE and AB-PAS staining, it could be confirmed that GPL mice were obviously reversed by Rg3. Additionally, the increased protein levels of PI3K, AKT, mTOR, HIF-1α, LDHA, and HK-II, which are crucial factors for evaluating GPL in the aspect of glycolysis pathogenesis in the model group, were downregulated by Rg3. Meanwhile, the miRNA-21 expression was decreased and upregulated by Rg3. Furthermore, the increased gene levels of Bcl-2 and caspase-3 were attenuated in Rg3-treated GPL mice. In conclusion, the findings of this study imply that abnormal glycolysis in GPL mice was relieved by Rg3 via regulation of the expressions of PI3K, AKT, mTOR, HIF-1α, LDHA, HK-II, and miRNA-21. Rg3 is an effective supplement for GPL treatment and can be harnessed to inhibit proliferation and induce apoptosis of GPL cells.
Highlights
Gastric cancer is a serious healthcare problem because of its high mortality rate [1, 2]
The findings of this study imply that abnormal glycolysis in Gastric precancerous lesions (GPLs) mice was relieved by Rg3 via regulation of the expressions of phosphoinositide 3-kinase (PI3K), AKT, mTOR, HIF-1α, lactate dehydrogenase A (LDHA), HK-II, and miRNA-21
We investigated the levels of proteins involved in the PI3K/AKT/ mTOR pathway, which were crucial factors for evaluating GPL in the aspect of glycolysis pathogenesis
Summary
Gastric cancer is a serious healthcare problem because of its high mortality rate [1, 2]. The prevalence in China is high, with 42% of all worldwide cases occurring in China [3]. Gastric precancerous lesions (GPLs) are a premalignant stage within Correa’s cancer cascade and are recognized as a point of no return for gastric carcinogenesis [4]. Various therapies exist for the treatment of GPL and gastric cancer, the therapies are less than satisfactory. This may be due to the multiple genetic variations and multiple altered microenvironments (such as altered glucose metabolism) that can promote gastric carcinogenesis
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