GEM on proliferation and apoptosis of childhood AL cells through inhibiting c‑myc expression by upregulating miR‑125a‑3p
- Weiwei Xing
- Yuxia Yin
- Saina Yang
- Guang Lu
Affiliations: Department of Pediatrics, Yidu Central Hospital of Weifang, Weifang, Shandong 262500, P.R. China, Department of Neurosurgery Ward II, Yidu Central Hospital of Weifang, Weifang, Shandong 262500, P.R. China, Department of Hematology, Shengli Oilfield Central Hospital, Dongying, Shandong 257034, P.R. China
- Published online on: February 14, 2020 https://doi.org/10.3892/ol.2020.11396
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Effect of gemcitabine (GEM) on proliferation and apoptosis of childhood acute leukemia (AL) cells and the mechanism of action were investigated. Bone marrow and peripheral blood of 18 newly diagnosed children with childhood AL admitted to Yidu Central Hospital of Weifang were selected, and the miR‑125a‑3p level in peripheral blood of healthy children and children with AL was detected by quantitative reverse transcription‑polymerase chain reaction (qRT‑PCR). Leukemia cells from the bone marrow of children with AL were primarily cultured and purified to observe the morphology. miR‑125a‑3p mimic was transfected into childhood AL cells. The cells were randomly divided into three groups: control group, GEM group and GEM + miR‑125a‑3p mimic group. 5‑ethynyl‑2'‑deoxyuridine (EdU) staining assay was chosen to detect the proliferation of childhood AL cells in each group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining assay was adopted to determine apoptosis of childhood AL cells. The protein level of c‑myc was measured via western blotting. Compared with that in the healthy children, the level of miR‑125a‑3p in the peripheral blood of children with AL was remarkably decreased. Compared with those in the control group, GEM inhibited proliferation and promoted apoptosis of childhood AL cells, and impeded the protein expression of c‑myc in these cells. Compared with those in the GEM group, GEM + miR‑125a‑3p mimic notably reduced the proliferation and enhanced apoptosis of cells, and the protein expression of c‑myc in cells was overtly reduced. The level of miR‑125a‑3p in peripheral blood of children with AL is obviously decreased. It is suggested in this study that GEM can inhibit the proliferation and promote apoptosis of childhood AL cells, and the mechanism may be related to upregulated miR‑125a‑3p inhibiting the expression of c‑myc.