Fig 1: GTPBP4 promoted NSCLC proliferation by regulating EMT. (a-b) The expression of E-cadherin protein was significantly increased, but the expression of Vimentin was significantly decreased in A549-sh-GTPBP4 group compared with the two control groups (n = 3 per group, ***P < 0.001, ###P < 0.001). (c-d) The expression of E-cadherin protein was significantly increased, but the expression of Vimentin was significantly decreased in Calu-1-sh-GTPBP4 group compared with the two control groups n = 3 per group, ***P < 0.001, ###(P < 0.001). (e-f) The expression of E-cadherin protein was also significantly increased and the Vimentin protein was significantly decreased in the LLC-GTPBP4 KO group compared with the LLC-WT group in mouse lung cancer tissue (n = 3 per group, **P < 0.01; ***P < 0.001).
Fig 2: The expression and diagnostic value of GTPBP4 in lung cancer. (a) GTPBP4 was upregulated in the majority of human cancer types available via TCGA, including LUAD. (b–e) GTPBP4 expression was increased in primary tumor LUAD samples compared to normal samples but has no statistically significant difference in T stage, lymph node metastasis status (N), distant metastasis status (M), and tumor pathological stage of lung cancer.(N0: no regional lymph node metastasis; N1: metastases in 1–3 axillary lymph nodes; N2: metastases in 4–9 axillary lymph nodes; M0: no distant metastasis; M1: distant metastasis). (f) The diagnostic value of GTPBP4 in lung cancer (**P < 0.01; ***P < 0.001).
Fig 3: Knockdown of GTPBP4 inhibited the invasive ability of A549 and Calu-1 cells. (a-b) The number of transmembrane cells in the sh-GTPBP4 group of A549 cells was significantly decreased compared with the control group, and the difference was statistically significant n = 3 per group, ∗∗∗P < 0.001, ###(P < 0.001); (c−d). The number of transmembrane cells in the sh−GTPBP4 group of Calu−1 cells was significantly decreased compared with the control group, and the difference was statistically significant (n = 3 per group, ∗∗∗P < 0.001, ###P < 0.001).
Fig 4: Poly-GR does not show co-localization with tested interactors in C9orf72 patient brain.(A) Immunofluorescent stainings of the frontal cortex of a C9orf72 patient and a healthy control case to analyze co-localization of poly-GR with the interacting proteins GTPBP4, NOP56, PRMT1, WDR77, MAGOHB, and TRA2A.
Fig 5: Knockout of GTPBP4 inhibited NSCLC proliferation in mice. (a) A mouse lung cancer model established by tail vein injection. At 21 days, the complete morphology of the lung tissue removed after the mice were sacrificed. (b) The lung weight of LLC-GTPBP4 KO mice was significantly reduced (n = 10 per group, **P < 0.01). (c) The number of lung tumor nodules in the LLC-GTPBP4 KO group was significantly less than that in the LLC-WT group (n = 10 per group, ***P < 0.001). (d) The volume of lung tumor nodules in the LLC-GTPBP4 KO group was significantly smaller than that in the LLC-WT group (n = 10 per group, ***P < 0.001).
Supplier Page from Abcam for Anti-GTPBP4/NOG1 antibody