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Published on: May 15, 2019
[The influence of bortezomib on HL-60 cell function induced by all-trans retinoic acid plus bufalin and its
Xiu-Juan Qu1, Yan-Ju Ma, Yun-Peng Liu
1Department of Medical Oncology, the First Hospital, China Medical University, Shenyang 110001, China.
Objective:
To investigate changes in the adherent ability, the expression of adhesion related proteins Pyk2 and paxillin during HL-60 cells differentiation into granulocyte-monocyte induced by low-dose (LD) bufalin in combination with all-trans retinoic acid (ATRA), and to explore the effects of bortezomib on cellular adhesion and the expression of Pyk2 and paxillin.
Methods:
The expression of CD11b was detected by flow cytometry, cellular adherence ability by MTT assay, and the expressions of Pyk2, paxillin and tubulin by Western blot.
Results:
The combination of 5 nmol/L bufalin and 30 nmol/L ATRA induced HL-60 cells differentiation in a time-dependent manner, the percentages of CD11b positive cells treated for 2 d and 4 d being (20.0 +/- 2.8)% and (75.0 +/- 5.3)%, respectively, with the increasing of cellular adherence ability. Meanwhile the expressions of Pyk2 and Paxillin were also up-regulated in a time-dependent manner. Bortezomib suppressed HL-60 cell adhesion in a dose-dependent manner. At concentrations of 1 nmol/L and 10 nmol/L the adherence level were (7.8 +/- 0.1)% and (5.3 +/- 0.3)%, respectively, with down-regulation of Pyk2 but not Paxillin.
Conclusion:
Pyk2 is involved in the regulation of cellular adherence function. Bortezomib might inhibit HL-60 cells adhension function by down-regulation of Pyk2 expression.
