Fig. 3: CS downregulates miR-1 specifically in the endothelial cells. | Communications Biology

Fig. 3: CS downregulates miR-1 specifically in the endothelial cells.

From: Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA

Fig. 3

A Human ex-vivo cultured lungs were treated with 1% CSE or vehicle (PBS) for 24 h, and epithelial (CD 45-, EPCAM +), endothelial (CD 45-, CD31 +), immune (CD 45 +), and double-negative (CD45−, CD31−) cells were isolated using magnetic sorting. The graph represents miR-1/reference gene levels in CSE-treated cellular fractions normalized to the levels in PBS groups and expressed as 2−∆∆Ct (n = 3 patients, *p = 0.0176). B–E Cells were treated with increasing concentrations of CSE for 24 h and miR-1/ reference gene levels were measured, normalized to the mean value of ‘0’ CSE concentration group (control), and expressed as 2−∆∆Ct (B) EA.hy926 (n = 21, 4, 18, and 9 from 4 experiments, *p = 0.0035, **p = 0.00145) (C) A549 cells (n = 6/concentration, from two experiments, *p = 0.0043) (D) HPMECs (n = 7 for 0 and 10% and 4 for 5%, from 2 experiments *p = 0.0012) (E) HUVECs (n = 11,10 and 8, from 3 experiments, *p = 0.007) (F) Endothelial cells were isolated from non-cancerous lung tissue (HPMECs) and tumor (TEC) from a lung cancer patient and cultured in growth media. miR-1/ reference gene levels were measured in total RNA from the cells, normalized to the mean levels in HPMEC group, and expressed as 2−∆∆Ct (n = 6, *p = 0.041).

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