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. 2021 Jan 1;11(6):2966–2986. doi: 10.7150/thno.48699

Figure 4.

Figure 4

SHMT2 maintains β-catenin stability by inhibiting its degradation. (A) RT-qPCR analysis of β-catenin in HCT116 and DLD-1 cells with siSHMT2 (n = 3). Ns: not significant; Student's t-test. (B) Western blot analysis (left) and quantification (right) of β-catenin in CRC cells after SHMT2 knockdown or SHMT2α overexpression. ** p < 0.01, *** p < 0.001; Student's t-test. (C) Western blot analysis (left) of SHMT2 and β-catenin after cell fractionation in HCT116 and DLD-1 cells with siSHMT2. Comparison of the relative reduction (right) of SHMT2 and β-catenin proteins in the cytoplasm and nucleus in CRC cells. (D) Western blot analysis (left) and quantification (right) of phosphorylated β-catenin after SHMT2 knockdown or SHMT2α overexpression in CRC cells. ** p < 0.05, *** p < 0.001; Student's t-test. (E) HCT116 (up) and DLD-1 cells (down) were treated with MG132 for 16 h and with siSHMT2 for 48 h. Cell proteins were subjected to immunoprecipitation using the indicated antibodies. (F) CRC cells stably expressing shNC or shSHMT2 were treated with MG132 for 16 h before harvesting. β-Catenin was immunoprecipitated and immunoblotted with the indicated antibodies. The data are presented as the mean ± SD from at least three independent experiments. The error bars show the SD.