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. 2020 Oct 19;11:569651. doi: 10.3389/fphar.2020.569651

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Copyright © 2020 Lin, Que, Lu, Li, Xiao, Zhu and Li

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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VPS9D1-AS1 promotes AML cell proliferation via the MEK/ERK signaling pathway. (A) Protein expression levels of key modulators of the MEK/ERK signaling pathway were analyzed by Western blotting in negative control (NC), VPS9D1-AS1-upregulated (VPS9D1-AS1UP), and VPS9D1-AS1-downregulated (VPS9D1-AS1KD) cells. (B) Correlation analysis between VPS9D1-AS1 and ERK/MEK signaling target genes. (C) Cell viability was measured after NC and VPS9D1-AS1-upregulated (VPS9D1-AS1UP) cells were treated with MEK/ERK signaling pathway inhibitor PD98059 (25 μM) for 48 h. ^* p < 0.05, ^** p < 0.01. (D) Cell cycle were analyzed by flow cytometry in NC and VPS9D1-AS1-upregulated (VPS9D1-AS1UP) cells were treated with PD98059 (25 μM) for 48 h. (E) Western blotting showed cell cycle protein expression in NC and VPS9D1-AS1-upregulated (VPS9D1-AS1UP) cells treated with PD98059 (25 μM) for 48 h.