Figure 4
CXCR2 is highly expressed in human leukemic cell lines and regulates viability in cell lines and primary samples. (A) qRT-PCR for CXCR2 demonstrates significantly increased expression in AML cell lines (t test, P < .05). (B) Viability of AML cell lines is inhibited by the CXCR2 inhibitor SB332235 compared with healthy CD34+ cells at 48 hours (t test, *P < .05, **P < .01). (C) Viability of primary MNCs from 2 AML and 2 high-risk MDS samples inhibited by the CXCR2 inhibitor. (D) shRNA against CXCR2 leads to significant knockdown by qRT-PCR in U937 cells (t test, P < .05). Colony growth shows significantly (E) decreased number and (F) size of leukemic colonies AML cells on CXCR2 knockdown compared with scrambled controls (t test, P < .01).

CXCR2 is highly expressed in human leukemic cell lines and regulates viability in cell lines and primary samples. (A) qRT-PCR for CXCR2 demonstrates significantly increased expression in AML cell lines (t test, P < .05). (B) Viability of AML cell lines is inhibited by the CXCR2 inhibitor SB332235 compared with healthy CD34+ cells at 48 hours (t test, *P < .05, **P < .01). (C) Viability of primary MNCs from 2 AML and 2 high-risk MDS samples inhibited by the CXCR2 inhibitor. (D) shRNA against CXCR2 leads to significant knockdown by qRT-PCR in U937 cells (t test, P < .05). Colony growth shows significantly (E) decreased number and (F) size of leukemic colonies AML cells on CXCR2 knockdown compared with scrambled controls (t test, P < .01).

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