期刊
CLINICAL AND TRANSLATIONAL MEDICINE
卷 12, 期 1, 页码 -出版社
JOHN WILEY & SONS LTD
DOI: 10.1002/ctm2.707
关键词
autophagy; circST3GAL6; FOXP2; gastric cancer; transcription factor
资金
- National Natural Science Foundation of China [81871946, 82072708]
- Special Foundation for National Science andTechnology Basic Research Program of China [2019FY101104]
- Primary Research & Development Plan of Jiangsu Province [BE2016786]
- Program for Development of Innovative ResearchTeam in the First Affiliated Hospital of NJMU
- PriorityAcademic Program Development of Jiangsu Higher Education Institutions [JX10231801]
- JiangsuKeyMedical Discipline [ZDXKA2016005]
- Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Centre for Cancer Personalized Medicine, Nanjing Medical University
In this study, it was found that circST3GAL6 was downregulated in gastric cancer and was associated with poor prognosis. Overexpression of circST3GAL6 inhibited malignant behaviors of gastric cancer cells, potentially through inducing apoptosis and autophagy. Furthermore, it was demonstrated that circST3GAL6 regulated gastric cancer through the miR-300/FOXP2 axis and regulated apoptosis and autophagy through FOXP2-mediated inhibition of the MET pathway.
Gastric cancer (GC) ranks third in mortality among all cancers worldwide. Circular RNAs (circRNAs) play an important role in the occurrence and development of gastric cancer. Forkhead box P2 (FOXP2), as a transcription factor, is closely associated with the development of many types of tumours. However, the regulatory network between FOXP2 and circRNAs remains to be explored. In our study, circST3GAL6 was significantly downregulated in GC and was associated with poor prognosis in GC patients. Overexpression of circST3GAL6 inhibited the malignant behaviours of GC cells, which was mediated by inducing apoptosis and autophagy. In addition, we demonstrated that circST3GAL6 regulated FOXP2 through the mir-300 sponge. We further found that FOXP2 inhibited MET Proto-Oncogene (MET), which was the initiating factor that regulated the classic AKT/mTOR pathway of autophagy. In conclusion, our results suggested that circST3GAL6 played a tumour suppressive role in gastric cancer through miR-300/FOXP2 axis and regulated apoptosis and autophagy through FOXP2-mediated transcriptional inhibition of the MET axis, which may become a potential target for GC therapy.
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