fig4

The antiangiogenic phloroglucinol hyperforin inhibits the secretion of proMMP-2, proMMP-9 and VEGF-A during apoptosis of primary acute myeloid leukemia cells

Figure 4. HF inhibits the production of proMMP-2/9 and VEGF-A by AML cells. (A) Total MMP-2 (n = 11), total MMP-9 (n = 8), and VEGF-A (n = 13) productions in the 72-h culture supernatants from AML samples untreated or treated with HF (2 μg/mL) were determined by ELISA. P value was calculated using a Mann-Whitney U-test; *P < 0.05; **P < 0.01. (B) The gelatinolytic activities of MMP-2/9 were analyzed using zymography (see Figure 2) in the supernatants from four AML cell samples treated or not with HF (2 μg/mL, 72 h). (C) PCR analyses of MMP-2, MMP-9, VEGF-A, and β2-microglobulin transcripts from 5 AML samples treated or not with HF (2 μg/mL, 24 h). (D) Correlations between the levels of HF-mediated release of MMP-2/9 or VEGF-A and HF-mediated death in AML cells (n = 11 for MMP-2; n = 8 for MMP-9; and n = 13 for VEGF-A). The percentage of HF-mediated AML cell death was determined as described in Figure 3. The percentage of HF-mediated release was determined by subtracting the percentage of MMP/VEGF-A release in the absence of HF from the percentage of MMP/VEGF-A release in the presence of HF, and then dividing by the percentage of MMP/VEGF-A release in the absence of HF × 100. Spearman’s correlation coefficient (r) and the P-value are shown.

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)

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