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Fig. 5 | Molecular Cancer

Fig. 5

From: Multi‑omics analysis identifies different molecular subtypes with unique outcomes in early-stage poorly differentiated lung adenocarcinoma

Fig. 5

Exploration the biological functions of GINS1 and CPT1C by in vitro and in vivo experiments. A, B Box plots showing statistical differences in GINS1 (A) and CPT1C (B) gene expression among normal and three subtypes (C1, C2 and C3) (C, D) Kaplan–Meier survival analysis of RFS comparing high and low expression levels of GINS1 (C) and CPT1C (D) gene (cutoff for each gene is detailed in the Methods). Hazard ratio, number of patients in each group, as well as p value are displayed. E, G The GINS1 (E) and CPT1C (G) knockdown efficiency was analyzed by western blotting in SPCA- 1 cells. F, H Transwell assay was performed to evaluate the effect of GINS1 (F) and CPT1C (H) depletion on migration and invasion ability of SPCA- 1 cells (n = 3). Representative images (left) and quantitative results (right). Scale bar, 200 µm. ***: p < = 0.001. I, K Colony formation assay was performed to evaluate the effect of GINS1 (I) and CPT1C (K) depletion on proliferation ability of SPCA- 1 cells (n = 3). **: 0.001 < p < = 0.01, ***: p < = 0.001. J, L CCK- 8 assay was performed to evaluate the effect of GINS1 (J) and CPT1C (L) depletion on cell viability of SPCA- 1 cells (n = 3). ***: p < = 0.001. M, N Images (left) and weight (right) of xenograft tumors derived from control SPCA- 1 cells and SPCA- 1 cells with GINS1 (M) or CPT1C (N) depletion (n = 5). ***: p < = 0.001.

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