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. 2020 Dec 3;12:12509–12517. doi: 10.2147/CMAR.S280554

Figure 1.

Figure 1

BCR-ABL regulates Alox12-12-HETE axis in human normal and malignant hematopoietic progenitor cells. (A) Alox12 and 12-HETE levels are higher in BP-CML (n=8) than NBM (n=5) CD34+ cells. (B) WB image shows Alox12 protein level in individual NBM and BP-CML CD34+ cells. (C) Quantification of WB shows average of Alox12 in NBM (n=2) and BP-CML (n=7) CD34+ cells. Overexpression of BCR-ABL in NBM CD34+ cells increased Alox12 protein level (D) and 12-HETE (E). BCR-ABL was transduced to NBM CD34+ cells. BCR-ABL knockdown by siRNA decreases Alox12 expression (F) and 12-HETE (G) in K562 cells. Cells are electroporated with 100 nM scramble or ABL siRNA. Image (H) and quantification (I) of WB shows decreased Alox12 in K562 cells after imatinib treatment. (J) Imatinib significantly decreases 12-HETE in K562 cells. Cells were harvested for WB and ELISA analysis after 24 hours treatment or 72 hours transfection. Densitometry was performed using Image J. *p<0.05, compared to NBM, p-Vec or 0 uM imatinib.