Journal
JOURNAL OF CANCER
Volume 12, Issue 15, Pages 4574-4584Publisher
IVYSPRING INT PUBL
DOI: 10.7150/jca.59138
Keywords
Mist1; gastric cancer; EMT; Wnt/beta-catenin signalling pathway
Categories
Funding
- National Natural Science Foundation of China [81502442]
- Fundamental Research Funds for the Central Universities of China [XJJ2018106]
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The study showed that overexpression of Mist1 could inhibit tumor growth and distant metastasis in gastric cancer by suppressing the Wnt/beta-catenin signaling pathway, suggesting Mist1 as a potential tumor suppressor and a novel marker for early gastric cancer screening.
As a secretory cell transcription factor, muscle intestine stomach expression 1 (Mist1) is associated with serous secretory cell development and gastric chief cell maturation. Here, we focus on the function of Mist1 in gastric adenocarcinoma carcinogenesis. Based on clinical data and a mouse model of gastric cancer, we found that Mist1 expression was reduced in gastric cancer. Then, we overexpressed Mist1 using a lentivirus system and found that overexpression of Mist1 could inhibit gastric cancer cell proliferation, migration and invasion in vitro. Additionally, in vivo, we assessed the function of Mist1 in a gastric cancer xenograft model and distant pulmonary metastasis model. Overexpression of Mist1 decreased tumour growth and distant metastasis in vivo, suggesting that Mist1 acts as a tumour suppressor in gastric carcinogenesis. Furthermore, Mist1 overexpression inhibited epithelial-mesenchymal transition (EMT) in gastric cancer by suppressing beta-catenin transcription activity and then the Wingless and INT-1 (Wnt)/beta-catenin signalling pathway, which could be reversed by a Wnt/beta-catenin-specific agonist. In conclusion, this study indicated that overexpression of Mist1 could reverse EMT in gastric carcinogenesis by inhibiting the Wnt/beta-catenin signalling pathway and that Mist1 might be a novel marker for early gastric cancer screening.
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