Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α
Bangyun Ma, Huibo Dai, Xingbin Dai, Shushu Qian, Xiaocao Sha, Xuemei Sun
Journal:Experimental and Therapeutic Medicine
IF:2.75
DOI:10.3892/etm.2022.11779
PMID:36684661
Published:2022-12-30
research field:肿瘤学分子生物学血液学
Abstract
The purpose of the present study was to evaluate cimigenol (Cim) treatment effects to cell proliferation by breaking bone marrow stromal cells (BMSCs) through C‑X‑C chemokine receptor type 4 (CXCR4)/stromal cell‑derived factor‑1α (SDF‑1α) pathway. MV‑4‑11 and U937 cell lines were used. The present study was divided into two parts. First, the cell lines were divided into normal control (NC), BMSC (cells co‑cultured with BMSCs), BMSC + DMSO, BMSC + Low (treated with 5 mg/ml Cim), BMSC + Middle (treated with 10 mg/ml Cim), BMSC + High (treated with 20 mg/ml Cim). In the second step, the cell lines were divided into NC, BMSC, BMSC + BL8040 (treated with BL8040 which inhibits CXCR4), BMSC + Cim and BMSC + Cim + BL8040. EdU positive cell numbers were measured by EdU assay and apoptosis rate by flow cytometry and TUNEL assay. Relative gene and protein expression was measured by reverse transcription‑quantitative PCR and western blotting assay. BMSCs were able to protect proliferation of cancer cells and decreased cell apoptosis compared with the NC group (P<0.001, respectively). With Cim supplement, the cell proliferation was decreased with cell apoptosis increasing compared with NC group (P<0.001 respectively). However, the anti‑tumor effects of Cim were not significantly different from the BL8040 treated groups (P<0.001, respectively). In conclusion Cim decreased acute myeloid leukemia cells protected by BMSCs through the CXCR4/SDF‑1α pathway.
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