[ARTICLE WITHDRAWN] Long Noncoding RNA MEG3 Inhibits Cell Proliferation and Metastasis in Chronic Myeloid Leukemia via Targeting miR-184

Abstract

THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN 03/2021. We submitted a manuscript entitled "Long Noncoding RNA MEG3 Inhibits Cell Proliferation and Metastasis in Chronic Myeloid Leukemia via Targeting miR-184", which was published in the 26(2) issue of Oncology Research. But now we found some inaccuracies in this manuscript. So after carefully thinking, we are going to withdraw manuscript and try to give more precise model. Thus we decided to withdraw this manuscript with great pity. We sincerely say sorry for all the staffs involved this manuscript because of our action. All authors agree to withdraw this manuscript. Thank you very much for your time and kind consideration. Thanks for your time and best wishes. Li Jingdong.

Figure 1

The expression of maternally expressed gene 3 (MEG3) is decreased in leukemia patients and cell lines. (A) The mRNA levels of MEG3 in serum from 57 leukemia patients were assayed by quantitative real-time polymerase chain reaction (qRT-PCR). (B) The mRNA levels of MEG3 in THP-1, HL-60, CCL-240, and CRL-1582 cells were assayed by qRT-PCR. All the experiments were repeated at least three times. *p < 0.05, **p < 0.01 versus normal cells or serum.

Figure 2

MEG3 overexpression suppresses proliferation and invasion of leukemia cells. (A) HL-60 cells were transfected with LV-GFP or LV-MEG3 for 24 h, and the mRNA levels of MEG3 were measured by qRT-PCR. (B) HL-60 cells were transfected with LV-GFP or LV-MEG3 for 24, 48, 72, and 96 h, and the cell viability was assayed by the CCK-8 kit. (C) Matrigel invasion assay. (D) Quantifications of (C). (E) Protein levels of proliferating cell nuclear antigen (PCNA), B-cell lymphoma 2 (BCL-2), matrix metalloproteinase 9 (MMP9), and vascular endothelial growth factor (VEGF) were assayed by Western blot. (F, G) Quantifications of (E). All the experiments were repeated at least three times, and the representative data are shown. GAPDH was used as loading control. *p < 0.05, **p < 0.01 versus mock.

Figure 3

MEG3 downregulates miR-184 expression in leukemia. (A) Bioinformatics analysis of MEG3 and miR-184. (B) HL-60 cells were transfected with luciferase reporter plasmid that contained the wild-type or mutant binding site of miR-184 and cotransfected with different levels of the miR-184 mimic for 24 h. Cell lysates were assayed for luciferase activity. (C) The mRNA levels of miR-184 in serum from 57 leukemia patients were assayed by qRT-PCR. (D) The mRNA levels of miR-184 in THP-1, HL-60, CCL-240, and CRL-1582 cells were assayed by qRT-PCR. (E) HL-60 cells were transfected with the LV-MEG3 and/or miR-184 mimic for 24 h, and the mRNA levels of miR-184 were assayed by qRT-PCR. (F) HL-60 cells were transfected with the MEG3 siRNA and/or miR-184 inhibitor for 24 h, and the mRNA levels of miR-184 were assayed by qRT-PCR. All the experiments were repeated at least three times. *p < 0.05, **p < 0.01, ***p < 0.001 versus normal cells or scramble. #p < 0.05 versus miR-184 mimic or inhibitor treated alone.

Figure 4

MEG3 downregulates miR-184 and mitigates the progression of leukemia. HL-60 cells were transfected with the LV-MEG3 and/or miR-184 mimic for 24 h. (A) Matrigel invasion assay. (B) Quantifications of (A). (C) Cell viability was assayed by the CCK-8 kit. (D) Mice were injected intraperitoneally with MEG3 overexpression or scramble HL-60 cells, and the tumor size was measured by ruler at 30 days. (E) Calculation of tumor volume at 6, 12, 18, 24, and 30 days after injection. (G, H) The expressions of MEG3 and miR-184 in tumor tissues were assayed by qRT-PCR. (I) Western blot analysis of PCNA and MMP9 in the tumor tissues. (J) Quantitation of (I). All the experiments were repeated at least three times. *p < 0.05, **p < 0.01 versus scramble. #p < 0.05 versus miR-184 mimic treated alone.