Journal
NEOPLASIA
Volume 22, Issue 5, Pages 220-230Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neo.2020.03.001
Keywords
MKL1; miR-5100; CAAP1; Autophagy; Apoptosis; Gastric cancer
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Funding
- National Natural Science Foundation of China [31501149, 31770815, 31570764]
- Hubei Natural Science Foundation [2017CFB537]
- Educational Commission of Hubei [B2017009]
- Hubei Province Health and Family Planning Scientific Research Project [WJ2017M173, WJ2019M255]
- Science and Technology Young Training Program of the Wuhan University of Science and Technology [2016xz035, 2017xz027]
- Innovation and Entrepreneurship Fund for Graduate of Wuhan University of Science and Technology [JCX2016024, JCX2017032, JCX2017033]
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Purpose: miR-5100 participates in the proliferation of lung cancer and pancreatic cancer cells, and participates in the differentiation of osteoblasts. However, the regulation of gastric cancer cells in gastric cancer cells remains unclear. Experimental design: The blood of patients was collected to detect the expression level of miR-5100, and the apoptosis and autophagy levels of cells were detected using western blot, flow cytometry, and confocal. At the same time, in vitro tumor formation experiments in nude mice were used to verify the results of in vitro experiments. Results: The expression of miR-5100 is related to the prognosis of gastric cancer, miR-5100 can enhance the apoptosis level of gastric cancer cells and inhibit the occurrence of autophagy by targeting CAAP1. MKL1 can inhibit the apoptosis of gastric cancer cells and promote the occurrence of autophagy by targeting CAAP1. At the same time, MKL1 can also increase the expression of miR-5100. Conclusions: Our research reveals the mechanism by which the MKL1/miR-5100/CAAP1 loop regulates apoptosis and autophagy levels in gastric cancer cells, and miR-5100 is expected to become a new potential target for gastric cancer treatment.
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