Cluster of Differentiation 47 (CD47) is regarded as a highly promising next-generation immunotherapy target following PD-1/PD-L1. It mediates tumor immune escape by transmitting a “don't eat me” signal through the signal regulatory protein alpha (SIRPα) pathway. However, the clinical application of existing antibody therapies remains constrained by erythrocyte toxicity, the antigen sink caused by widespread CD47 expression on normal cells, and recent setbacks in clinical trials. "Growing evidence establishes non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as key upstream regulators of CD47. Here, we systematically review how these ncRNAs control CD47 gene expression, focusing on their impact on phagocytosis, drug resistance, and tumor microenvironment remodeling. Unlike antibody-mediated blockade, targeting the ncRNA–CD47 axis provides a unique avenue for genetic modulation, offering reduced systemic toxicity. We summarize these regulatory mechanisms and explore how exploiting these gene-regulatory networks can address the current challenges in CD47 immunotherapy.

This study elucidates a novel mechanism by which the natural product berberine (BBR) reverses methicillin-resistant Staphylococcus aureus (MRSA) resistance to β-lactam antibiotics. It was established that BBR interferes with the BlaR1/BlaI regulatory pathway by means of downregulating the signal sensor gene blaR1 and the repressor gene blaI, thereby significantly suppressing the expression of the β-lactamase-encoding gene blaZ at the transcriptional level. The combination susceptibility testing demonstrated that BBR and Oxacillin exhibited synergistic or additive effects in 76.92

Background : Irinotecan is a commonly used chemotherapeutic drug for pancreatic cancer (PC), but its specific mechanism of inducing cell death is yet to be elucidated. Exosomes are key mediators of intercellular communication and are involved in tumorigenesis. This study aimed to investigate whether irinotecan-induced ferroptosis can inhibit PC progression, and to explore the mechanism of exosomes derived from PC cells reverse irinotecan-induced ferroptosis. Methods : Exosomes were isolated from cells via polymer precipitation method. CCK8 assay and colony formation assay were used to test the proliferation of PC cells. Wound-healing assay and Transwell migration assay were used to test the migration of PC cells. Ferroptosis in cells was detected by analysis of malondialdehyde, glutathione, Fe2+ and reactive oxygen species concentrations. Transmission electron microscopy was used to observe the morphology of intracellular mitochondria. Related proteins were detected by Western blot. Results : Irinotecan could inhibit the proliferation of PC cells, decrease the expression of the ferroptosis-negative regulators glutathione peroxidase 4 and cystine transporter solute carrier family 7 member 11, and increase the intracellular concentrations of Fe2+ and ferroptosis metabolites. However, exosomes derived from PC cells inhibit irinotecan-induced ferroptosis and diminish the anti-tumor effect, whereas this effect was significantly reduced following the knockdown of hnRNPA2B1. Conclusions : These findings indicated that exosomal hnRNPA2B1 could inhibit irinotecan-induced ferroptosis of PC, which strongly regulated the progression and drug resistance of PC.

Clinical management of inflammatory bowel disease (IBD) is hampered by limited therapeutic targets, primary non-response, secondary loss of efficacy, and safety risks, which undermine clinical outcomes. Probiotics and postbiotics represent promising preclinical candidates to alleviate these unmet clinical bottlenecks. Bacterial extracellular vesicles (BEVs) are naturally secreted bacterial nanovesicles carrying abundant bioactive cargos, whose bioactivity and safety are highly strain-dependent. Probiotics-derived BEVs can remodel gut homeostasis, repair epithelial barriers, and regulate mucosal immunity to suppress the inflammatory vicious cycle in IBD, while pathogen-/pathobiont-derived BEVs loaded with lipopolysaccharide and virulence factors exacerbate intestinal inflammation. Native BEVs are restricted by low cargo loading, poor gastrointestinal stability and inadequate colon tropism. Rational engineering strategies, including surface modification, self-loading hybridization, genetic manipulation, and pH-responsive coating, can optimize the therapeutic performance of BEVs. This review systematically summarizes BEVs biological mechanisms, engineering approaches, and translational obstacles and outlines prospects for the design of intelligent multifunctional BEVs and standardized large-scale manufacturing as future directions, providing theoretical support for oral BEVs nanotherapies against IBD.

Methicillin-resistant Staphylococcus aureus (MRSA) infection remains a major global health challenge, with its high pathogenicity largely attributed to a wide array of virulence factors. The accessory gene regulator (Agr) quorum-sensing system acts as a central hub for regulating virulence gene expression in MRSA, making it an attractive target for anti-virulence therapeutic strategies. This study investigated the inhibitory effect of the natural compound berberine (BBR) on MRSA virulence. Quantitative Real-time polymerase chain reaction (qRT-PCR) revealed that BBR significantly suppressed Agr system activity, leading to marked downregulation of key virulence genes, including α-Hemolysin (also known as α-toxin or Hla), Phenol-soluble modulin α (psmα), and Clumping factor A (clfA). Phenotypic assays confirmed that BBR treatment reduced hemolytic activity, biofilm formation, and host cell invasion. In a murine model of MRSA-induced pneumonia, BBR provided notable protective effects, as evidenced by reduced lung tissue damage, diminished inflammatory cell infiltration, and preservation of alveolar structure. Furthermore, BBR attenuated excessive production of pro-inflammatory cytokines and chemokines. Collectively, these findings demonstrate that BBR suppresses MRSA virulence by targeting the Agr quorum-sensing system. This highlights its potential as a novel anti-virulence agent or as a complementary approach to conventional antibiotic therapy, offering a promising strategy for managing MRSA infections.

Cancer remains a major threat to human health, with chemotherapy serving as one of the main treatment strategies to alleviate patient suffering. However, prolonged chemotherapy often leads to the development of drug resistance, complicating treatment outcomes. Cisplatin, a commonly utilized chemotherapeutic agent, demonstrates efficacy against a range of cancers but frequently encounters resistance, posing a significant challenge in tumor management and prognosis. Drug resistance not only facilitates tumor progression but also reduces survival rates, highlighting the urgent need for innovative strategies to overcome this issue. In recent years, non-coding RNAs, particularly circular RNAs (circRNAs), have gained attention in cancer therapy due to their stability and specificity. Moreover, an increasing number of studies have reported that circRNAs are involved in cisplatin resistance across various types of cancer. This paper primarily reviews the mechanisms and roles of circRNA in mediating cisplatin resistance over the past 3 years. These findings highlight circRNAs as promising therapeutic targets for overcoming cancer drug resistance.

IntroductionBreast cancer is one of the most common cancers in women and poses a serious threat to women's health. Circular RNAs (circRNAs) have been found to be specifically expressed in cancers and regulate the growth and death of tumor cells. The role of circRNAs in breast cancer remain unknown. In this study, we explored the impacts of circRNAs on the progression of breast cancer cells.MethodsUsing bioinformatics analysis, we screened out one up-regulated circRNA in breast cancer, and its function and regulatory mechanisms were confirmed by quantitative real-time PCR, cell counting kit-8 experiment, migration assay, dual luciferase reporter assay, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, cell immunofluorescence, clone formation assay, scratch wound healing experiment, RNA immunoprecipitation and subcutaneous tumor-bearing experiments.ResultsCirc_0022382 was highly expressed in breast cancer cell lines MDA-MB-231, MCF-7 as well as breast cancer tissues, and promoted the proliferative and migratory capacity of breast cancer cells. In terms of regulatory mechanisms, circ_0022382 activated PI3K/AKT/mTOR signaling pathway and SLC7A11 by sponging let-7a-5p, while knockdown of circ_0022382 contributed to the occurrence of disulfidptosis. In addition, EIF4A3 promoted the expression of circ_0022382 in MDA-MB-231 and MCF-7. Consistently, knockdown of circ_0022382 inhibited the growth of breast cancer cells in vivo.DiscussionCirc_0022382 and its related molecules may be effective targets for diagnosis or targeted therapy of breast cancer.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that a pair of data panels appeared to contain overlapping data in each of Fig. 3A and C on p. 1473, showing the results of Transwell migration and scratch‑wound assay experiments respectively, where the data panels were intended to have shown the results from differently performed experiments; moreover, control GAPDH western blotting data featured in Fig. 4B and 5A appeared to be matching, albeit the bands had been inserted into these figure parts in reversed orientations. The authors were able to re‑examine their original data, and realized that errors had occurred in the assembly of these figures through mislabelling of certain of their data files. Owing to the time that had passed since this paper was published, the authors offered to repeat the affected experiments, and the revised versions of Figs. 3, 4 and 5, showing new data for Figs. 3A, 3C, 4B and 5A, are shown on the next two pages. Given that the new experiments yielded data that were not significantly different from those obtained previously, the authors wish to emphasize that the re‑presentation of these figures with the new data does not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this corrigendum, and all the authors agree with the publication of this corrigendum; moreover, they apologize to the readership for any inconvenience caused. [Oncology Reports 34: 1469‑1477, 2015; DOI: 10.3892/or.2015.4109].

The migrasome, a recently discovered organelle formed during cell migration, is a membrane-bound vesicular structure containing numerous smaller intracavitary vesicles and cellular contents. It is generated at the tips and intersections of retraction fibers (RFs). Upon the rupture of RFs, migrasomes can either be engulfed by surrounding cells or undergo lysis to release their contents into the extracellular microenvironment. The process through which cells release their contents via migrasomes is termed migracytosis. Migrasomes play crucial roles in intercellular signaling, cellular homeostasis maintenance, and intercellular material transport. This article provides a comprehensive review of the discovery, biogenesis, isolation and characterization, biological functions of migrasomes, as well as their roles in the occurrence, progression, diagnosis, and treatment of clinical diseases. Furthermore, this paper proposes novel hypotheses and future directions regarding the current research challenges of migrasomes and their potential clinical applications, which may facilitate future clinical diagnosis and treatment involving migrasomes.

The initiation and progression of breast cancer generally involve complex immune regulatory mechanisms, with increased expression of programmed cell death ligand 1 (PD-L1) as an essential factor for immune evasion and the formation of a tumor-promoting immune microenvironment. Emerging evidence underscores the regulatory role of non-coding RNAs (ncRNAs) in modulating PD-L1 expression, influencing immune evasion, tumorigenesis, and therapy resistance in breast cancer. Therefore, it is crucial further to clarify alternative regula-tory mechanisms that control PD-L1 expression. The variations in PD-L1 expression among different breast cancer subtypes and the mechanisms by which ncRNAs regulate the expres-sion of PD-L1 are delineated. This study explores the potential and challenges of combining ncRNA-based therapy with PD-L1 inhibitors, offering insights into PD-L1 regulation and per-sonalized treatment strategies in breast cancer.

Abstract Breast cancer is one of the most common cancers in women and poses a serious threat to women's health. In this paper, we examined the role of circular (circ)RNA in breast cancer, and screened out circ_0022382 for high expression in breast cancer by differential analysis of breast cancer and adjacent tissues in the GEO database. The high expression of circ_0022382 in breast cancer cell lines MDA-MB-231, MCF-7 as well as breast cancer tissues was confirmed by qRT-PCR. The proliferation, migration and apoptosis of MDA-MB-231 and MCF-7 breast cancer cells were significantly increased by transfection of siRNA targeting circ_0022382, and dual luciferase reporter assays showed that circ_0022382 bound to microRNA (miR) let-7a-5p. Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analysis predicted that the mammalian target of rapamycin (mTOR) and phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathways were the main pathways regulated by let-7a-5p. The addition of let-7a-5p inhibitor reduced the proliferation and migration of breast cancer cells caused by circ_0022382 knockdown by rescuing the expression of p-AKT. Let-7a-5p also directly regulates the expression of cystine transporter solute carrier family 7 member 11 (SLC7A11) proteins, and through examination of glucose in cell supernatants and the addition of cystine inhibitors (dithiothreitol), we found that this process was closely related to disulfidptosis. In addition, eukaryotic translation initiation factor 4A3 (EIF4A3) promoted increased expression of circ_0022382 in breast cancer cells. In conclusion, EIF4A3-induced circ_0022382 regulates the expression of SLC7A11 proteins and related proteins in the PI3K-AKT signaling pathway by sponging let-7a-5p, which affects glucose metabolism and induces the death of breast cancer cells. Therefore, circ_0022382 may be useful as a marker or therapeutic agent in breast cancer treatment.

Abstract Vascular endothelial cells are closely related to tumor progression, and extracellular vesicles (EVs) play an important role in this process. EVs derived from breast cancer cells also affect the biological characteristics of human umbilical vein endothelial cells (HUVECs) to promote tumor progression. However, the mechanism remains unclear. In the present study, EVs derived from MDA-MB-231 and MCF-7 breast cancer cells were extracted at different concentrations (0, 10, 20, and 40 μg/ml). Specific concentrations of breast cancer cell line EVs (10, 20, and 40 μg/ml) significantly increased the proliferation, Colony formation, and migration of HUVECs (P < 0.05) compared to MDA-MB-231 and MCF-7 breast cancer cell-derived EVs. There was no significant difference in the expression levels of total JAK2 and STAT3 protein (P < 0.05), while the expression levels of P-JAK2 and P-STAT3 protein increased significantly (P < 0.05). In conclusion, EVs derived from breast cancer cells may promote the proliferation and migration of HUVECs by regulating the phosphorylation of the JAK2/STAT3 signaling pathway.

目的:探究circ_0000515 在乳腺癌进展中的可能作用机制.方法:通过GEO数据库下载乳腺癌circRNA芯片数据集(GSE101123)并采用R语言进行表达差异分析,筛选出目标circRNA分子作为研究对象并检测其在乳腺癌细胞株和组织中的表达;生物信息学分析与选择该circRNA的目的miRNA,及后者对应的靶向mRNA,并采用双荧光素酶实验和蛋白质印迹进行验证;将目标circRNA的siRNA转染人乳腺癌MCF-7 和MDA-MB-231 细胞,CCK-8 实验和划痕实验观察细胞的增殖和迁移,荧光定量PCR(qRT-PCR)检测RNA表达,蛋白质印迹实验检测mRNA编码蛋白的表达.结果:选择和下载GSE101123 数据集后用R语言筛选出 5 个高表达的circRNA分子,选定其中的circ_0000515 作为研究对象,生物信息学分析得出circ_0000515、miR-1296-5p和细胞周期蛋白依赖性激酶2(cyclin-dependent kinase 2,CDK2)三者之间可能存在靶向关系.qRT-PCR结果显示,circ_0000515 中乳腺癌细胞株MCF-7 和MDA-MB-231 中的表达明显高于人乳腺上皮细胞株MCF-10A;在乳腺癌组织中的表达明显高于癌旁组织中的表达.抑制circ_0000515 表达后,乳腺癌细胞增殖和迁移能力较对照组显著下降,miR-1296-5p表达明显增高;双荧光素酶实验证实 circ_0000515 与 miR-1296-5p 之间存在靶向关系.蛋白质印迹实验证实抑制 circ_0000515 表达后CDK2 蛋白表达明显减低.结论:circ_0000515 在乳腺癌中高表达,可能通过circ_0000515/miR-1296-5p/CDK2 作用轴影响乳腺癌进展.

目的:探究邻苯二甲酸二(2-乙基己基)酯(di-2-ethylhexyl phthalate,DEHP)损伤小鼠GC-1 spg精原细胞功能的可能机制.方法:采用不同浓度DEHP(0、30、60、90、120 μmol/L)处理GC-1 spg细胞,通过CCK8 实验、克隆形成实验和Transwell实验检测细胞增殖和迁移能力的变化;化学分光光度比色法检测细胞内铁离子(Fe3+)和丙二醛的相对含量;蛋白质印迹实验检测细胞内铁死亡相关蛋白胱氨酸/谷氨酸逆转运蛋白(xCT)和谷胱甘肽过氧化物酶4(GPX4)的相对表达;细胞免疫荧光染色技术检测细胞内活性氧水平以及线粒体膜电位(JC-1)的改变.使用铁死亡抑制剂Ferrostatin-1(1 μmol/L)与DEHP(90 μmol/L)联合培养GC-1 spg细胞24 h,CCK8 实验检测细胞的增殖能力.结果:与对照组(0 μmol/L)相比,30、60、90、120 μmol/L DEHP组细胞的增殖能力、克隆形成能力和迁移能力明显下降;丙二醛、活性氧、Fe3+(90、120 μmol/L DEHP组)含量明显升高;线粒体膜电位(60、90、120 μmol/L DEHP组)明显降低;GPX4(60、90、120 μmol/L DEHP组)和xCT蛋白表达水平明显降低.DEHP与Ferrostatin-1 联合培养后细胞增殖能力较DEHP单独培养明显提高.结论:DEHP能够抑制GC-1 spg细胞的增殖和迁移能力,降低GPX4 和xCT蛋白的表达,可能通过铁死亡途径引起细胞死亡.

OBJECTIVE:To explore mutational characteristics of acute myeloid leukemia (AML) patients with CBFβ-MYH11+ and analyze the correlation between the mutations and partial clinical characteristics.METHODS:A total of 62 AML patients with CBFβ-MYH11+ were included and 51 candidate genes were screened for their mutations using targeted next-generation sequencing (NGS). The exon 12 of NPM1 , FLT3-ITD , and TAD, bZIP domains of CEBPA were detected by genomic DNA-PCR combined with sanger sequencing.RESULTS:Compared with RUNX1-RUNX1T1 + group, the patients with CBFβ-MYH11+ showed higher age, peripheral WBC level, initial induced complete remission (CR) rate, more commonly carried chromosomal abnormalities such as +22, and lower deletion ratio of sex chromosome (-X or -Y) (P<0.05). In AML patients with CBFβ-MYH11+, the most common mutation was NRAS , followed by KIT, KRAS , and FLT3-TKD . Compared with RUNX1-RUNX1T1+ group, NRAS and FLT3-TKD were more frequently mutated in patients with CBFβ-MYH11+ (51.6% vs 18.7%, 17.7% vs 3.8%) (P<0.05).CONCLUSION:The genomic landscape and clinical characteristics of AML patients with CBFβ-MYH11+ are different from patients with RUNX1-RUNX1T1 +.

目的:构建尼古丁诱导的小鼠生精细胞体外损伤模型,探讨小鼠骨髓间质干细胞来源的胞外囊泡(mouse bone marrow mesenchymal stem cell-derived extracellular vesicles,mBMMSCs-EVs)对于小鼠GC-1生精细胞损伤的修复作用.方法:采用不同浓度尼古丁(0、8、16、32μg/mL)处理GC-1生精细胞24、48、72 h,通过MTT实验筛选尼古丁诱导GC-1生精细胞损伤的最适浓度和时间;将GC-1生精细胞分为对照组、尼古丁组、尼古丁+胞外囊泡组;通过MTT实验、Transwell实验和流式细胞术凋亡实验观察mBMMSCs-EVs干预前后受损生精细胞GC-1生物学特性的变化.结果:MTT实验结果表明,32μg/mL尼古丁作用GC-1生精细胞24 h时,细胞增殖能力明显降低(P<0.05),mBMMSCs-EVs作用于尼古丁预处理后,细胞增殖能力明显增高(P<0.05);与对照组相比,尼古丁组GC-1生精细胞迁移能力明显降低,细胞凋亡能力明显升高(P均<0.01),与尼古丁组相比,尼古丁+胞外囊泡组生精细胞增殖和迁移能力明显升高,细胞凋亡能力明显下降(P<0.01或<0.05).结论:mBMMSCs-EVs可以逆转尼古丁引发的GC-1生精细胞增殖、迁移能力的损伤以及细胞凋亡.

Abstract Objective: To investigate the effect and mechanism of breast cancer cell-derived extracellular vesicles (EVs) on the biological characteristics of Human umbilical vein endothelial cells (HUVECs). Methods: MDA-MB-231 and MCF-7 breast cancer cell-derived EVs were extracted to treat HUVECs with different concentrations (0, 10, 20 and 40 μg/mL) respectively for different times. The proliferation was detected by MTT assay and plate clone formation assay. Transwell assay was used to detect the migration and invasion，scratch wound assay was used to detect the migration and Western blotting was to detect related protein expression of JAK2/STAT3 signaling pathway. Results: Compared with 0μg/mL MDA-MB-231 and MCF-7 breast cancer cell-derived EVs, the specific concentration (10, 20 and 40 μg/mL ) of breast cancer cell-derived EVs improved the proliferation, plate cloning and migration of HUVECs significantly (P<0.05); there was no significant difference in total JAK2 and STAT3 protein expression (P<0.05), while the expression of p-JAK2 and p-STAT3 protein increased significantly (P<0.05).Conclusion: Breast cancer cell-derived EVs might promote the proliferation and migration of HUVECs by regulating the phosphorylation of JAK2/STAT3 signaling pathway.

目的:探讨小鼠脂肪间质干细胞(adipose-derived mesenchymal stem cells,ADSCs)源胞外囊泡(extracellular vesicles,EVs)对卵巢癌ID8细胞株生物功能的影响及其可能机制.方法:采用酶消化法分离获得ADSCs,利用其形态特征、成骨成脂多向分化能力和流式细胞术表面标志检测对ADSCs进行鉴定;采用超速离心法从ADSCs上清液中分离和纯化EVs(ADSC-EVs),并通过透射电子显微镜、纳米粒径分析和蛋白质印迹实验进行鉴定;以PBS作为对照组,实验组采用不同浓度ADSC-EVs(20μg/mL和40μg/mL)分别预处理ID8细胞,通过平板克隆实验检测ADSC-EVs对ID8细胞增殖能力的影响;划痕实验和Transwell实验检测ADSC-EVs对ID8细胞迁移能力的影响;蛋白质印迹实验检测ID8细胞上皮间质转化(epithelial-mesenchymal transition,EMT)和蛋白激酶B(即AKT)相关蛋白的表达.结果:分离的ADSCs具有典型的干细胞形态,能够向成骨成脂分化,并符合干细胞表面一般特征;ADSC-EVs表达CD9和CD81蛋白;与PBS组相比,ADSC-EVs组ID8细胞增殖和迁移能力明显增强(P均<0.05),且40μg/mL ADSC-EVs组细胞增殖和迁移能力较20μg/mL ADSC-EVs组明显增强(P均<0.05);随着ADSC-EVs浓度增加,ID8细胞E-钙黏蛋白表达明显降低,N-钙黏蛋白、波形蛋白和p-AKT表达明显增加(P均<0.05).结论:ADSC-EVs可能通过激活AKT信号的磷酸化促进ID8细胞EMT,进而增强其增殖和迁移能力.

目的:探讨miR-376c-3p在乳腺癌中的表达水平、生物学功能及分子调控机制.方法:通过实时荧光定量PCR检测乳腺上皮MCF-10A细胞及乳腺癌细胞中miR-376c-3p表达水平;然后,用miR-376c-3p mimic转染乳腺癌MCF-7与MDA-MB-231细胞,用平板克隆实验、划痕实验以及Transwell实验分别检测其增殖与迁移能力.利用Starbase数据库预测miR-376c-3p的下游靶基因,并通过蛋白质印迹实验进行验证.结果:与人乳腺上皮MCF-10A细胞相比,乳腺癌MCF-7和MDA-MB-231细胞中miR-376 c-3p表达水平显著降低(P＜0.01);平板克隆实验显示,过表达miR-376c-3p可以显著抑制乳腺癌细胞增殖(P均＜0.05);Transwell实验和划痕实验表明,miR-376c-3p表达上调可抑制乳腺癌细胞迁移能力;通过生物信息学预测分析,结果显示miR-376 c-3p可以与谷氨酸受体相互作用蛋白1(glutamate receptor interacting protein 1,GRIP1)结合,且蛋白质印迹实验证实过表达miR-376c-3p可以抑制乳腺癌细胞GRIP1表达,同时波形蛋白表达水平明显下调,E-钙黏蛋白表达明显上调.结论:在乳腺癌细胞中,miR-376c-3p表达下调;在体外,过表达miR-376c-3p可显著抑制乳腺癌细胞的增殖和迁移能力,可能通过靶向GRIP1调节乳腺癌细胞上皮间质转化进程.

Platelet-rich plasma (PRP) and its byproduct platelet-poor plasma (PPP) are rich sources of cytokines in tissue damage repair. Bone marrow-derived mesenchymal stem cells (BM-MSCs) have received more and more attention for their ability to treat multiple diseases. The purpose of our study was to investigate the biologic action of PPP and PRP on BM-MSCs. The adipogenic potential of BM-MSCs revealed no obvious change, but the osteogenic ability of BM-MSCs was enhanced after treated with PRP. CCK8 assays and cell colony formation assays showed that PRP promoted cell proliferation, while this effect of PPP was not obvious. No obvious difference was found in cell cycle and apoptosis of BM-MSCs between PRP and PPP treatment. Expression of β-galactosidase, a biological marker of senescence, was decreased upon PRP treatment which indicated that PRP provided significant protection against cellular senescence. The migratory capacity of BM-MSCs was detected by scratch and transwell assays. The results indicated that PRP could affect the migration ability of BM-MSCs. From immunofluorescence detection and western blot, we demonstrated that the level of epithelial-mesenchymal transition-related proteins was changed and several pluripotency marker genes, including Sox2, Sall4, Oct4, and Nanog, were increased. Finally, the expression of the key signal pathway such as PI3K/AKT was examined. Our findings suggested that PRP promoted cell migration of BM-MSCs via stimulating the signaling pathway of PI3K/AKT.