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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: TPI1 activates the PI3K/AKT/mTOR signaling pathway to induce breast cancer progression by stabilizing CDCA5

Fig. 2

TPI1 promotes proliferation, migration, invasion and aerobic glycolysis in BRCA in vitro. A TPI1 protein and mRNA expression levels were determined in T47D cells (left panel) by stably expressing control vector or shTPI1 (shTPI1-1, 2, 3, respectively) and in MDA-MB-231 cells (right panel) by stably expressed empty vector or TPI1, shTPI1-2 and shTPI1-3 (sh2, sh3) were relatively effective at knocking down. β-actin served as a control. B Cellular viability of T47D/sh2, sh3 and T47D/NC (left panel), MDA-MB-231/TPI1 (right panel) and vector control were analyzed by CCK-8 assays. C Colony forming assays were conducted in T47D/sh2, sh3 and T47D/NC (left panel), MDA-MB-231/TPI1 (right panel) and vector control. D Edu assays were conducted in T47D (left panel) and MDA-MB-231 (right panel) cells. E Transwell assays were conducted to assess cell migration and invasion after knockdown or overexpression of TPI1, respectively, in T47D (left panel) and MDA-MB-231 (right panel) cells compared with corresponding vector cells. F Wound healing assays were performed in T47D (left panel) and MDA-MB-231 (right panel) cells. G, H Relative glucose uptake (G) and lactate production (H) were determined in T47D and MDA-MB-231 cells. I Western blot analysis of indicated proteins in TPI1 knockdown and TPI1 overexpression cells, respectively. β-Actin served as a control. Experiments were performed at least three times. Data were presented as the means ± SEMs (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001)

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