LINC00641 contributes to nasopharyngeal carcinoma cell malignancy through FOXD1 upregulation at the post-transcriptional level

2021 ◽  
pp. 1-9
Author(s):  
Dan Ren ◽  
Jinlong Lu ◽  
Xing Han ◽  
Weiming Xiong ◽  
He Jiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Tumor Promoter ◽  
Luciferase Reporter ◽  
Blue Staining ◽  
Transcriptional Level ◽  
Functional Analyses ◽  
Rip Assay

Nasopharyngeal carcinoma (NPC) is a common tumor in the head and neck and is prevalent in China, especially in the southern regions. Molecular mechanisms have attracted much attention in NPC research. FOXD1 has been reported to be a tumor promoter in various cancers. The present study was designed to explore the function of FOXD1 in NPC cells. Functional analyses, including the trypan blue staining assay, EdU and JC-1 assay, and flow cytometry analysis, revealed that FOXD1 facilitated NPC cell proliferation and inhibited NPC cell apoptosis. Next, by means of “starBase” database and mechanism analyses, such as RIP assay, RNA pull-down assay and luciferase reporter assay, miR-378a-3p was found to target FOXD1 and negatively regulate FOXD1 expression in NPC cells. Moreover, miR-378a-3p plays a suppressive role in NPC cells. LINC00641 was identified as a sponge of miR-378a-3p and positively modulated FOXD1 expression in NPC cells. Finally, a series of rescue assays indicated that LINC00641 accelerated NPC cell proliferation and hindered NPC cell apoptosis through FOXD1 upregulation. In conclusion, the present study demonstrated an innovative ceRNA mechanism of LINC00641/miR-378a-3p/FOXD1 in NPC cells, which might provide new insights into NPC treatment.

scholarly journals MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Cartilage Cells ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes

Abstract Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms, in osteoarthritis (OA). Methods: Cartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate construct, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1 . Western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model. Results: Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, using western blot analyses and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix. Conclusion: MEG3 can contribute to cell proliferation and inhibit cell apoptosis and degradation of extracellular matrix (ECM) via the miR-361-5p/FOXO1 axis in OA chondrocytes.

scholarly journals Circ-FOXM1 Promotes Cell Proliferation, Migration and EMT Process in Osteosarcoma Through FOXM1-Mediated Wnt Pathway Activation

2021 ◽  
Author(s):  
Hao Zhang ◽  
Qiongqiong Zhou
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Biological Activities ◽  
Wnt Signaling Pathway ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Transcriptional Level ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells

Abstract Background: As the most common primary bone tumor in adolescents and children, osteosarcoma commonly occurs with high mortality rate and metastasis. Emerging evidence has illustrated that circular RNAs (circRNAs) are important regulatory RNAs that are involved in multiple biological activities of carcinomas. Circ-FOXM1 (hsa_circ_0025033) is a recently found circRNA and promotes the cellular activities of several cancers. However, the function and molecular mechanism of circ-FOXM1 in osteosarcoma have not been interrogated yet. Methods: The qRT-PCR was utilized to test the expression of circ-FOXM1 in osteosarcoma cell lines. Loss-of-function assays including CCK-8, EdU, TUNEL, transwell and western blot assays were conducted to measure cell proliferation, cell migration, EMT process and cell apoptosis. Luciferase reporter assay and RIP assay were utilized to detect the interaction of circ-FOXM1 and RNAs. Results：We discovered the high expression of circ-FOXM1 in osteosarcoma cells. Besides, it was indicated that circ-FOXM1 knockdown inhibited cell proliferation, cell migration and EMT process, as well as induced cell apoptosis of osteosarcoma cells. Furthermore, circ-FOXM1 was discovered to upregulate the expression level of forkhead box M1 (FOXM1) at post-transcriptional level. Moreover, it was proved that circ-FOXM1 sponged miR-320a and miR-320b so as to increase FOXM1 expression. Additionally, circ-FOXM1 could activate Wnt signaling pathway through upregulating FOXM1. In the end, rescue assays certified that FOXM1 overexpression could totally rescue the circ-FOXM1 silence-repressed cellular activities of osteosarcoma cells.Conclusion: Circ-FOXM1 facilitated the progression of osteosarcoma cells via relieving FOXM1 from the inhibition by miR-320a and miR-320b.

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p. Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Normal Group ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes

Abstract Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were enrolled in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. After different transfections, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. The qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis of cartilage cells. Histological analysis and immunostaining were conducted in OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes.

scholarly journals miR-331-3p Inhibits Proliferation and Promotes Apoptosis of Nasopharyngeal Carcinoma Cells by Targeting elf4B-PI3K-AKT Pathway

2020 ◽  
Vol 19 ◽  
pp. 153303381989225 ◽  
Author(s):  
Zhang Xuefang ◽  
Zheng Ruinian ◽  
Jiang Liji ◽  
Zhang Chun ◽  
Zheng Qiaolan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Apoptosis ◽  
Target Gene ◽  
Regulation Of Gene Expression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Clinical Samples ◽  
Phosphoinositide 3 Kinase

Background: The incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide. Objectives: Although previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma. Materials and Methods: Real-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression. Results: The expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT). Conclusion: miRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway. Significance: The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.

scholarly journals MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Cartilage Cells ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes

Abstract Background This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms, in osteoarthritis (OA). Methods Cartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate constructs, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model. Results Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, using western blot analyses and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix. Conclusion MEG3 can contribute to cell proliferation and inhibit cell apoptosis and degradation of extracellular matrix (ECM) via the miR-361-5p/FOXO1 axis in OA chondrocytes.

scholarly journals MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Normal Group ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes

Abstract Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The RT-qPCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Moreover, western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Finally, rat model analysis showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes.

scholarly journals The LncRNA MIR503HG/miR-224-5p/TUSC3 Signaling Cascade Suppresses Gastric Cancer Development via Modulating ATF6 Branch of Unfolded Protein Response

2021 ◽  
Vol 11 ◽  
Author(s):  
Han Lin ◽  
Jinge Wang ◽  
Tong Wang ◽  
Jiaming Wu ◽  
Peng Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Unfolded Protein Response ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Blue Staining ◽  
Signaling Cascade ◽  
Mesenchymal Transition ◽  
Unfolded Protein ◽  
Protein Response

BackgroundUnfolded protein response (UPR)-mediated tumor-promoting functions have been identified in multiple cancers, and this study focused on investigating the role and molecular mechanisms of UPR in modulating gastric cancer (GC) pathogenesis.MethodsThe bioinformatics analysis was performed to examine the expression status of cancer associated genes in patients with stomach adenocarcinoma (STAD) and predict the targeting sites of miR-224-5p with LncRNA MIR503HG and TUSC3. Genes expressions were quantified by Real-Time qPCR, Western Blot and immunohistochemistry (IHC). Cell proliferation, viability, apoptosis and mobility were evaluated by MTT assay, trypan blue staining assay, flow cytometer and transwell assay, respectively. The binding sites were validated by dual-luciferase reporter gene system assay.ResultsLncRNA MIR503HG and TUSC3 were downregulated, but miR-224-5p was upregulated in GC tissues and cells, in contrast with their normal counterparts. Further gain- and loss-of-function experiments validated that the malignant phenotypes in GC cells, including cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and tumorigenesis, were negatively regulated by LncRNA MIR503HG. Mechanistically, LncRNA MIR503HG upregulated TUSC3 in GC cells through sponging miR-224-5p, resulting in the repression of GC progression. Finally, we validated that knock-down of ATF6, but not other two branches of UPR (PERK1 and IRE1), partially rescued cell proliferation and EMT in the GC cells with LncRNA MIR503HG overexpression.ConclusionsTargeting the LncRNA MIR503HG/miR-224-5p/TUSC3 signaling cascade suppressed ATF6-mediated UPR, resulting in the blockage of GC development.

scholarly journals MEG3 inhibits proliferation and promote apoptosis in osteoarthritis chondrocytes by miR-361-5p/wnt/β-catenin axis

2019 ◽  
Author(s):  
Anying Wang ◽  
Naixia Hu ◽  
Yefeng Zhang ◽  
Yuanzhen Chen ◽  
Changhui Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Control Group ◽  
Oa Chondrocytes ◽  
Inhibit Cell Proliferation

Abstract Background: This study aimed to investigate the role of long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and control group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The cells transfected with pcDNA3.1-NC and pcDNA3.1-MEG3, and then cultured with XAV939 was named as pcDNA3.1-NC +XAV939 group and pcDNA3.1-MEG3 + XAV939 group respectively. The RT-qPCR was used to detect the expression of MEG3 and miR-361-5p . Moreover, Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of lncRNA MEG3 and miR-361-5p in OA was significantly decreased and increased respectively than that in normal. Meanwhile, MEG3 was competitive binding with miR-361-5p in OA chondrocytes. Moreover, the Western blot and CCK-8 assay showed that MEG3 might inhibit cell proliferation and promote cell apoptosis via Wnt/β-catenin pathway. Finally, rat model analysis showed that MEG3 contributed to the cartilage matrix degradation. Conclusion: MEG3 and miR-361-5p might down-regulated and up-regulated respectively in the chondrocytes of OA patients. Furthermore, MEG3 might inhibit cell proliferation and promote cell apoptosis via miR-361-5p/Wnt/β-catenin axis in OA chondrocytes.

scholarly journals MicroRNA-223 decreases cell proliferation, migration, invasion, and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O 1

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Chunyu Li ◽  
Tana Zhao ◽  
Lei Nie ◽  
Yanhong Zou ◽  
Quan Zhang
Keyword(s):  
Cell Proliferation ◽  
Acute Lymphoblastic Leukemia ◽  
Protein Expression ◽  
Mrna Expression ◽  
Cell Apoptosis ◽  
Target Gene ◽  
Molecular Mechanisms ◽  
Lymphoblastic Leukemia ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Objective: Acute lymphoblastic leukemia (ALL) is a frequent malignancy in childhood. The present study was aimed to investigate the effect of miR-223 in ALL and its underlying molecular mechanisms. Methods: The mRNA expression of miR-223 and FOXO1 was detected by qRT-RCR in ALL children. The correlation between miR-223 and clinical indexes of ALL was determined. CCRF-CEM and NALM-6 cells were transfected with miR-223 mimic and miR-223 inhibitor, respectively. The proliferation, apoptosis, invasion and migration of CCRF-CEM and NALM-6 cells were measured by MTT, flow cytometry and transwell assay. The protein expression of FOXO1 was detected by Western blot. Additionally, dual-luciferase reporter and RNA pull-down assay were performed to investigate the target gene of miR-223 and validate their targeting relationship. Results: The mRNA expression of miR-223 was markedly down-regulated in ALL, but FOXO1 was up-regulated. The protein expression of FOXO1 was highly expressed in CCRF-CEM and NALM-6 cells. The expression of miR-223 was related to WBC, PLT, RBC and risk stratification. Overexpression of miR-223 not only inhibited cell proliferation, migration and invasion, but also induced cell apoptosis. Importantly, FOXO1 was a target gene of miR-223 in ALL cells. Silencing of FOXO1 reversed the effects of miR-223 inhibitor on cell proliferation, migration, invasion and apoptosis in ALL. Conclusions: miR-223 could inhibit cell proliferation, migration and invasion, and promote apoptosis by targeting FOXO1 in ALL.

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