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. 2019 Feb 8;10(12):1238–1249. doi: 10.18632/oncotarget.26664

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Copyright: © 2019 Al-Haidari et al.

This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

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(A) Conditioned media from neutrophils stimulated with CXCL-2 and co-incubated with vehicle or DNase I (50 μg) was used to study colon cancer cell migration as described in Materials and Methods. Migration was quantified by counting cells in 10 High Power Fields in 5 different fields. Migration index was calculated as the ratio of the number of migrated cells divided by the number of cells in the insert wells. (B) Representative images showing colon cancer cell migration. (C, D) CT-26 cell surface expression of αv and β3 integrins. (E) Conditioned media from neutrophils stimulated with CXCL-2 and co-incubated with vehicle, the CXCR2 antagonist (SB225022), anti-CD51 antibody or DNase I (50 μg) was used to study colon cancer cell adhesion to vitronectin as described in Materials and Methods. Data represents mean ± SEM and n = 5.

(A) Conditioned media from neutrophils stimulated with CXCL-2 and co-incubated with vehicle or DNase I (50 μg) was used to study colon cancer cell migration as described in Materials and Methods. Migration was quantified by counting cells in 10 High Power Fields in 5 different fields. Migration index was calculated as the ratio of the number of migrated cells divided by the number of cells in the insert wells. (B) Representative images showing colon cancer cell migration. (C, D) CT-26 cell surface expression of αv and β3 integrins. (E) Conditioned media from neutrophils stimulated with CXCL-2 and co-incubated with vehicle, the CXCR2 antagonist (SB225022), anti-CD51 antibody or DNase I (50 μg) was used to study colon cancer cell adhesion to vitronectin as described in Materials and Methods. Data represents mean ± SEM and n = 5.