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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Norepinephrine-stimulated HSCs secrete sFRP1 to promote HCC progression following chronic stress via augmentation of a Wnt16B/β-catenin positive feedback loop

Fig. 1

NE activates HSCs through α1A-ADR. a, b HSCs express a high level of a subtype of adrenergic receptors, α1A-ADR. The expression of α1A-ADR was significantly increased in HSCs (LX-2 and p-HSC) compared with HCC cells, as analyzed by qRT–PCR and western blot analysis. c Immunofluorescent staining of α1A-ADR in HSCs (LX-2 and p-HSC) (magnification, × 100). d, e Pretreated with α1-ADR antagonist prazosin (10 μM) or selective α1A-ADR antagonist 5-methylurapidi (5-Mu) (5 μM), LX-2 cells were exposed to 10 μM NE for 24 h. The mRNA and protein levels of αSMA and COL1A1 were determined by qRT-PCR analysis and western blot analysis. f, g Pretreated with α1-ADR antagonist prazosin or selective α1A-ADR antagonist 5-methylurapidi (5-Mu), LX-2 cells were treated with 10 μM NE for 24 h. Cell proliferation was measured by CCK-8 assay. Cell apoptosis was detected by flow cytometry using Annexin V/PI staining. h Protein expression levels of cyclinD1 and cleaved caspase 3 were determined by western blot analysis in LX-2 cells pretreated with prazosin or 5-Mu prior to 10 μM NE treatment. **P < 0.01, *** P < 0.001

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