Objective To investigate the effect of silent proline⁃rich protein 13 (PRR13) gene on proliferation and apoptosis of colorectal cancerous cells, and to explore its possible mechanism based on autophagy⁃associated proteins, immune cell⁃associated cytokines, and Wnt/β⁃catenin signaling pathway. Methods (1) The mRNA expression of PPR13 in normal human colorectal epithelial cells (FHC cell), and in human colorectal cancerous cells (HCT116 cell, HT⁃29 cell, LS174T cell, SW480 cell, SW620 cell, LoVo cell, and HR⁃8348 cell) were detected, after then human colorectal cancerous cells with the highest expressions were selected to perform follow⁃up experiment. (2) HR⁃8348 cell was assigned to control group, empty vector group, PRR13⁃small interfering RNA (siRNA) group, IWR⁃1 group, or PRR13⁃siRNA+IWR⁃1 group. The control group did not received any intervention, whereas the empty vector group was transfected with negative control siRNA, the PRR13⁃siRNA group was transfected with PRR13⁃siRNA, the IWR⁃1 group received IWR⁃1 intervention of Wnt/β⁃catenin signaling pathway inhibitor, and the PRR13⁃siRNA+IWR⁃1 group was transfected with PRR13⁃siRNA and received IWR⁃1 intervention. PPR13 mRNA expression, cell survival rate, cell apoptosis rate, γ⁃interferon level, interleukin (IL)⁃4 level, and expressions of microtubule⁃associated protein 1 light chain 3 Ⅱ (MAP1LC3Ⅱ ), Beclin 1 protein, β⁃catenin protein, glycogen synthase kinase 3β (GSK⁃3β) protein, and Wnt11 protein were detected in various groups. Results (1) Except for SW620 cell, PRR13 mRNA expression of the remaining 6 human colorectal cancerous cells was all higher than that of human colorectal epithelial FHC cell, and PRR13 mRNA expression in HR⁃8348 cell was higher than that in the remaining human colorectal cancerous cells (P<0.05). (2) Compared with the control group and the empty vector group, the remaining 3 groups yielded decreased PRR13 mRNA level, cell survival rate, and IL⁃4 level, as well as down⁃regulated expressions of MAP1LC3Ⅱ protein, Beclin 1 protein, β⁃catenin, GSK⁃3β protein, Wnt11 protein, and elevated cell apoptosis rate and γ⁃interferon expression (P<0.05). Compared with the PRR13⁃siRNA group and the IWR⁃1 group, the PRR13⁃siRNA+IWR⁃1 group exhibited more significant changes of the aforementioned indices (P<0.05), but there was no statistically significant difference in the aforementioned indices between the PRR13⁃siRNA group and the IWR⁃1 group (P>0.05). Conclusion Silent PRR13 gene can inhibit colorectal cancerous cell activity, and promote its apoptosis. Its mechanism may by related to regulate Th differentiation, inhibit autophagy⁃associated protein activity, and activate Wnt/β⁃catenin signaling pathway. Combining the inhibition of the Wnt/β⁃catenin signaling pathway with silent PRR13 gene may provide a better anti⁃colorectal cancer effect.

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