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. 2024 May 15;22:460. doi: 10.1186/s12967-024-05284-7

Fig. 2.

Fig. 2

Loss of CCT6A inhibits the proliferation of LUAD in vitro and in vivo (A-B) Colony formation assays and growth curves (days 1–4) represented the proliferation of A549/PC9 cells infected with sh-NC or sh-CCT6A. Representative images of the crystal violet staining of cells in a 6-well plate and statistics were shown. (C) CCT6A knockdown resulted in increased apoptosis in LUAD cells. Representative FACS images and statistics based on three independent experiments were shown. (D) Transwell assays were performed to assess the migration of A549/PC9 cells infected with sh-NC or CCT6A-sh-1/2. Cells crossing the membrane were dyed with crystal violet (10×magnification). Scale bars = 100 μm. (E) Migration of A549/PC9 cells with CCT6A knockdown was assessed using wound healing assays. Area coverages were observed at 48 h (10× magnification). Scale bars = 100 μm. (F) Representative images of subcutaneous tumors on the left flank of mice injected with sh-NC or sh-CCT6A A549 cell (n = 5, each group). (G) Tumor growth curves were plotted every 5 days to 25days. (H) The weight of tumors was measured. (I) Representative images of IHC staining for CCT6A and Ki67 proteins (20×magnification). Scale bars = 100 μm. * P < 0.05; ** P < 0.01; *** P < 0.001. Variables are presented as mean ± SD