Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/ijms23094787
Keywords
miR-5100; LEF1-AS1; DEK; autophagy; apoptosis
Funding
- Hubei Provincial Health Commission [WJ2021Q051]
- Wuhan Science and Technology Bureau [2020020601012250]
- Hubei Provincial Department of Education, Hubei Provincial Department of Education Science and Technology Research Program Guidance Project [B2020001]
- Wuhan University of Science and Technology Graduate Innovation and Entrepreneurship Fund Project [JCX2020060]
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DEK and miR-5100 play critical roles in gastric cancer, with DEK regulating autophagy and apoptosis through the AMPK/mTOR pathway, and miR-5100 promoting apoptosis and inhibiting autophagy by targeting DEK. LEF1-AS1 has opposite effects on autophagy and apoptosis compared to miR-5100.
DEK and miR-5100 play critical roles in many steps of cancer initiation and progression and are directly or indirectly regulated by most promoters and repressors. LEF1-AS1 as a long non-coding RNA can regulate tumor development through sponge miRNA. The effect and regulatory mechanism of DEK on autophagy and apoptosis in gastric cancer (GC), and the role between miR-5100 and DEK or miR-5100 and LEF1-AS1 are still unclear. Our study found that DEK was highly expressed in gastric cancer tissues and cell lines, and knockdown of DEK inhibited the autophagy of cells, promoted apoptosis, and suppressed the malignant phenotype of gastric cancer. DEK regulates autophagy and apoptosis through the AMPK/mTOR signaling pathway. In addition, miR-5100 inhibits autophagy and promotes apoptosis in GC cells while LEF1-AS1 had the opposite effect. Studies have shown that miR-5100 acts by targeting the 3 ' UTR of DEK, and LEF1-AS1 regulates the expression of miR-5100 by sponging with mIR-5100. In conclusion, our results found that LEF1-AS1 and miR-5100 sponge function, and the miR-5100/DEK/AMPK/mTOR axis regulates autophagy and apoptosis in gastric cancer cells.
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