Affiliation:
1. Department of Gastrointestinal Surgery The First Affiliated Hospital of Baotou Medical College Baotou China
2. Department of Gastrointestinal Surgery Qi Lu Hospital of Shandong University Jinan China
3. Department of General Surgery HeNan RongJun Hospital Xinxiang China
Abstract
AbstractIntroductionThe purpose of this research was to determine how the P53/microRNA‐34a (miR‐34a)/survivin pathway contributes to oxaliplatin‐induced (L‐OHP) cell inhibition in gastric cancer.MethodsThe BGC‐823 gastric cancer cells were selected, and we examined their viability following treatment with L‐OHP at different concentrations and time periods. The expression levels of miR‐34a, P53, and survivin in the cells were determined.ResultsIn the 12‐ and 24‐h groups, drug concentration of 15 μg/cm² (p < .005 in both) significantly lowered cell viability. In comparison to the control group, miR‐34a mRNA expression, P53 mRNA expression, and protein expression were all significantly greater in the 24‐h group (p = .0324, p = .0069, p = .0260, respectively), but survivin mRNA and protein expressions were significantly lower than those in the control group (p = .0338, p = .0032, respectively). There was a significant decrease in gastric cancer cells in the miR‐34a overexpression group (p = .0020), a significant increase in P53 mRNA and protein expression compared to the control group (p = .0080, p = .0121, respectively), and a significant decrease in survivin mRNA and protein expression compared to the control group. (p = .0213, p = .0069, respectively).ConclusionOxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR‐34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR‐34a/survivin axis) in BGC‐823 gastric cancer cells.