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. 2022 Sep 10;56:102458. doi: 10.1016/j.redox.2022.102458

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© 2022 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 2 — GTPBP4 promotes HCC growth and metastasis. (A) GTPBP4-OE PLC/PRF/5 and GTPBP4‐KD HCCLM3 cells were constructed by transfecting overexpressing lentivirus and shRNA and were validated by western blotting and qRT-PCR. n = 3, unpaired 2-tailed t-test. (B) Evaluation of the influence of GTPBP4 overexpression and knockdown on the proliferation of PLC/PRF/5 and HCCLM3 cells by CCK-8. n = 6, one-way ANOVA. (C) The influence of GTPBP4 overexpression and knockdown on migratory and invasive capacities of PLC/PRF/5 and HCCLM3 cells was evaluated by transwell assays. n = 3, one-way ANOVA or unpaired 2-tailed t-test. (D) Evaluation of the influence of GTPBP4 overexpression and knockdown on apoptosis in PLC/PRF/5 and HCCLM3, respectively, was determined by flow cytometry. n = 3, unpaired 2-tailed t-test. (E) Subcutaneous xenograft mouse models were constructed using PLC/PRF/5 Vector or PLC/PRF/5-GTPBP4 cells. Tumor growth curves (middle) and weight (right) are shown. n = 6, unpaired 2-tailed t-test. (F) Subcutaneous xenograft mouse models were constructed by using HCCLM3-Control or HCCLM3-shGTPBP4. Tumor growth curves (middle) and weight (right) are shown. n = 6, Error bars represent the mean ± SD from three or more independent experiments. **P < 0.01, ***P < 0.001; unpaired 2- tailed t-test.