Fig 1: The expression levels of PGC-1ß and FOXA2 in breast cancer tissues and cells. a The expression levels of PGC-1ß and FOXA2 in breast cancer tissues and matched adjacent tissues by qRT-PCR. b, c The expression levels of PGC-1ß and FOXA2 mRNA and proteins were detected by qRT-PCR and western blot. d Representative pictures of PGC-1ß and FOXA2 expression by immumohistochemical staining in breast cancer and non-cancer tissues (PGC-1ß expression in non-cancer tissues: a ×40, b ×400; PGC-1ß expression in breast cancer tissues: c ×40, d ×400; FOXA2 expression in non-cancer tissues: e ×100, f ×400; FOXA2 expression in breast cancer tissues: g ×100, h ×400). e Subcellular localization of PGC-1ß and FOXA2 were detected by immunofluorescence staining. (MCF-7: original magnification ×630, scale bar = 10 µm; MDA-MB-231: original magnification ×400, scale bar = 20 µm). All values were expressed as mean ± SD. *P < 0.05, **P < 0.01
Fig 2: The formation and identification of ovine UGs organoids. (A) The formation of UGs organoids in Matrigel. (B) The identification of organoids by cytokeratin (green) and FOXA2 (red) immunoreactivity. Bar = 100 µm.
Fig 3: FOXA2 protects hepatocytes against apoptosis in fibrotic livers. (a) TUNEL assay indicating the DNA strand breaks in fibrotic livers. The cell nuclei were counterstained using DAPI (blue). Right panel: Quantification of the apoptotic cells. Scale bars, 50 µm. (b,c) Western blot analysis of the levels of Bax and cleaved caspase-3 in the liver lysates. (d) The immunohistochemistry staining for cleaved caspase-3 was quantified by Image-Pro Plus 6 software (right). More cytoplasmic staining for cleaved caspase 3 was observed at the periphery of the centrilobular areas of CCl4-treated FOXA2H-KO livers. Representative images are shown (n = 6 mice in per biological group). Scale bars, 50 µm. (e,f) Western blotting was performed to analyse the levels of apoptosis-regulated proteins, Bax and cleaved caspase 3 from fibrotic liver lysates in AAV-TBG/AAV-TBG-FOXA2 groups. (g) The in situ analysis of cleaved caspase-3 levels in AAV-TBG-Control or AAV-TBG-FOXA2-treated fibrotic livers (n = 8–10 mice in each group). Data are shown as the mean ± SD. ***P < 0.001.
Fig 4: Hepatocyte-specific overexpression of FOXA2 alleviates liver fibrosis. (a) The hepatocyte-specific FOXA2 overexpression model was generated by injecting virus AAV8-TBG-FOXA2 via the tail vein in C57Bl/6 J mice 1 week after the first CCl4 injection. Mice were sacrificed 5 weeks after CCl4 administration. (b) Immunofluorescence staining showed the expression of FOXA2 and a-SMA. More staining for FOXA2 was located in hepatocytes after FOXA2 gene delivery. Scale bars, 50 µm. (c) Immunohistochemistry staining for FOXA2 and a-SMA. H&E and Sirius red staining were performed to evaluate the pathological alterations and ECM deposition. Scale bars, 50 µm. (d) Semi-quantitative analysis of Sirius red staining of the livers from each group mice. (e) The amount of hydroxyproline in mouse livers. (f,g) The protein levels (f) and the mRNA levels (g) of FOXA2 and fibrogenic genes (Col1a1 and Acta2) in mouse livers (n = 8–10 mice in each group). *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 5: Model of context-specific regulation of lung cancer identity by NKX2-1, FoxA1 and FoxA2.SCJ: squamocolumnar junction of GI tract.
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