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Fig. 3 | Stem Cell Research & Therapy

Fig. 3

From: Alpha-enolase (ENO1), identified as an antigen to monoclonal antibody 12C7, promotes the self-renewal and malignant phenotype of lung cancer stem cells by AMPK/mTOR pathway

Fig. 3

ENO1 promoted the self-renewal, growth, and invasion ability of LCSCs. Lung cancer stem cells (LCSCs) were enriched from GV248-ShENO1B or GV358-ENO1 transfected SPCA-1 and A549 cells. a Sphere formation assay demonstrated that the sphere formation abilities of two transfected LCSCs were both inhibited by ENO1 knockdown (right panel) but enhanced by ENO1 overexpression (left panel). Scale bar, 100 μm. b Colony formation assay demonstrated that the cell growth abilities of two transfected LCSCs were both inhibited by ENO1 knockdown (right panel) but enhanced by ENO1 overexpression (left panel). c Matrigel-coated Transwell assay demonstrated that the cell invasion ability of two transfected LCSCs were both inhibited by ENO1 knockdown (right panel) but enhanced by ENO1 overexpression (left panel). Scale bar, 100 μm. Data are expressed as mean ± SEM of three independent experiments. *p < 0.05, **p < 0.01, compared to control (CON)

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Stem Cell Research & Therapy

ISSN: 1757-6512