期刊
DRUG DEVELOPMENT RESEARCH
卷 81, 期 5, 页码 544-550出版社
WILEY
DOI: 10.1002/ddr.21650
关键词
AMPK; mTOR; chemotherapy resistance; gastric cancer; TRIM14
资金
- Discipline Construction Program of Pudong New District Health Bureau [PWZbr2017-01]
- Pudong New District Health Bureau Project [PW2019A-18]
- Shanghai Municipal Commission of Health and Family Planning Project [201840290]
Objective To study the relationship between TRIM14 expression and chemotherapy resistance of gastric cancer (GC) cells. Methods The expression of TRIM14 in 5-fluorouracil (5-FU)- and oxaliplation (L-OHP)-resistant GC tissues and cells were determined by qRT-PCR and western blotting. PcDNA3.1-TRIM14 and shRNA-TRIM14 vector were transfected to 5-FU-resistant GC cells (SGC7901/5-FU), and the proliferation and apoptosis of cells were measured. Animal experiments on 5-FU-resistant GC mice were performed to study the effect of TRIM14 expression on tumor size and weight, GC cell migration, and proliferation. pcDNA3.1-MK-3903 plasmid was transfected to SGC7901/5-FU cells with TRIM14 silence. The cell proliferation and apoptosis were determined. The protein expressions of Trim14, LC3, and BECLIN1 were measured by western blotting. Results TRIM14 was significantly upregulated in 5-FU- and L-OHP-resistant GC tissues and cells. The overexpression of TRIM14 promoted the proliferation and autophagy of SGC7901/5-FU cells, and inhibited the apoptosis. Moreover, in vivo experiment verified that the silence of TRIM14 reduced the tumor size and weight, and inhibited the migration and proliferation of GC cells in 5-FU-resistant GC mice. The overexpression of MK-3903 reversed the inhibiting role of TRIM14 knockout on the proliferation and autophagy of SGC7901/5-FU cells. Conclusion TRIM14 promoted chemotherapy resistance of GC cells by regulating AMPK/mTOR pathway, and may be a new biomarker for treating GC.
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