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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Knockdown of HMGA2 regulates the level of autophagy via interactions between MSI2 and Beclin1 to inhibit NF1-associated malignant peripheral nerve sheath tumour growth

Fig. 2

HMGA2 knockdown directly leads to the inhibition of human NF1 MPNST cell growth via G0/G1 arrest and apoptosis. a and b Two shHMGA2 sequences were used to knock down HMGA2 expression in sNF96.2 cells. Both protein and mRNA HMGA2 expression levels were significantly decreased upon transfection with shHMGA2. c and d HMGA2-encoding sequences were used to overexpress HMGA2 in NFSCs. HMGA2 expression was significantly increased at both the protein and mRNA levels upon transfection with HMGA2 expression constructs. e EdU (red) assays for proliferation rates. Nuclei are stained with Hoechst 33342 (blue). Scale bar = 50 μm. f Graphical representation of the proportions of EdU-positive sNF96.2 and ST8814 cells transfected with shScr or shHMGA2. shHMGA2 shows fewer EdU positive cells, indicating that shHMGA2 inhibits cell growth. g Cell viability evaluated by the CCK-8 assay. shHMGA2 cells show lower cell viability compared to shScr cells. h and i Cell cycle analysis performed using FCM. More shHMGA2 cells are in G0/G1 stage compared to shScr cells. j Percentage of apoptotic cells determined by FCM. shHMGA2 induces apoptosis more than shScr. k Effects of HMGA2 knockdown on G0/G1 phase- and apoptosis-related proteins, as assayed by WB. Each data point is presented as the mean ± SD. *P < 0.05. All experiments were performed in three biological replicates

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