scholarly journals Adiponectin Protects against Glutamate-Induced Excitotoxicity via Activating SIRT1-Dependent PGC-1αExpression in HT22 Hippocampal Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Liang Yue ◽  
Lei Zhao ◽  
Haixiao Liu ◽  
Xia Li ◽  
Bodong Wang ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Critical Role ◽  
Tunel Staining ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Expression Levels

Glutamate- (Glu-) induced excitotoxicity plays a critical role in stroke. This study aimed to investigate the effects of APN on Glu-induced injury in HT22 neurons. HT22 neurons were treated with Glu in the absence or the presence of an APN peptide. Cell viability was assessed using the MTT assay, while cell apoptosis was evaluated using TUNEL staining. Levels of LDH, MDA, SOD, and GSH-Px were detected using the respective kits, and ROS levels were detected using dichlorofluorescein diacetate. Western blot was used to detect the expression levels of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), cleaved caspase-3, Bax, and Bcl-2. In addition to the western blot, immunofluorescence was used to investigate the expression levels of SIRT1 and PGC-1α. Our results suggest that APN peptide increased cell viability, SOD, and GSH-Px levels and decreased LDH release, ROS and MDA levels, and cell apoptosis. APN peptide upregulated the expression of SIRT1, PGC-1α, and Bcl-2 and downregulated the expression of cleaved caspase-3 and Bax. Furthermore, the protective effects of the APN peptide were abolished by SIRT1 siRNA. Our findings suggest that APN peptide protects HT22 neurons against Glu-induced injury by inhibiting neuronal apoptosis and activating SIRT1-dependent PGC-1αsignaling.

Inhibition of autophagy sensitizes gastrointestinal stromal tumor cells to TKI/Bcl-2 inhibitors-induced apoptosis.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 11036-11036
Author(s):  
Shuchao Zhang ◽  
Guozhi HU ◽  
Ana Cristina Paz-Mejia ◽  
Luyuan Li ◽  
Jonathan C. Trent
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Tumor Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Kinase Inhibitor ◽  
Synergistic Effects ◽  
Critical Role ◽  
Drug Combinations ◽  
Cell Viability Assay

11036 Background: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the GI tract. Most GISTs are driven by mutations in KIT or platelet-derived growth factor receptor-α (PDGFRA), which responds well to imatinib, a tyrosine kinase inhibitor (TKI) that blocks KIT and PDGFR-α signaling. Bcl-2 family plays a critical role in the regulation of cell apoptosis in GISTs. ABT-737 as an inhibitor of Bcl-2/Bcl-xL can result in a time and dose-dependent activation of apoptosis. Autophagy is a key mechanism to promote tumor cells survival, inhibition of which can induce the cell death in GISTs. Chloroquine, an antimalarial drug, has been also identified as an autophagy inhibitor. In this study, we assessed the combinational effects of imatinib, ABT-737 and chloroquine in GIST cells. Methods: Human GIST cell lines, GIST-T1 and GIST-882, were employed in our study. Cells were treated with imatinib, ABT-737 and chloroquine either separately or in different combinations. Cell viability was tested by means of MTS and synergistic effects were analyzed by isobologram software. The levels of related proteins of apoptosis (PARP, Caspase-3) and autophagy (LC3-II, beclin-1) were measured by western blot. Cell apoptosis and cell cycle were tested by flow cytometry. Results: Cell viability assay indicated cell survival percentage of double or triple drug combinations ( < 5%) dramatically decreased compared to single drug treatments (42%, 36% or 12%) ( P< 0.05). Isobologram analysis revealed triple drugs combination had stronger synergistic effects than double drugs combinations (CI = 0.204 vs 0.309 or 0.356, P< 0.05). Cell apoptosis percentage of double (32.9% or 36.6%) or triple drugs combinations (66.5%) significantly increased compared to single treatments (6.1%, 6.1% or 13.1%) ( P< 0.05). Western blot showed drugs combinations increased cleavage of PARP and Caspase-3 levels, but inhibited autophagy. Conclusions: The combination of imatinib, ABT-737 and chloroquine has collaborative effects on the treatment of GISTs in vitro. The combined strategy may enhance the clinical efficacy, which provides a rationale for the clinical evaluation of these drug combinations in GISTs treatment.

scholarly journals Rhodioloside inhibits apoptosis of hippocampal neurons exposed to sevoflurane via cAMP/PKA signaling pathway

2020 ◽  
Vol 19 (9) ◽  
pp. 1827-1834
Author(s):  
Yuqiang Su ◽  
Yan Bai ◽  
Zhonglei Zheng ◽  
Xiaoying Fan
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Control Group ◽  
Sprague Dawley ◽  
Expression Levels ◽  
Inhalational Anesthetics ◽  
Pathway Activation ◽  
Pka Pathway

Purpose: Neural injury affects patients after using inhalational anesthetics such as sevoflurane. Rhodioloside, a compound which is obtained from the Rhodiola rosea plant has been implicated to be the most commonly used psychostimulant that can improve a range of conditions. The study was aimed at finding the molecular mechanism underlying the Rhodioloside treatment of sevoflurane-injured hippocampal neurons.Methods: Main hippocampal neurons, secluded from Sprague Dawley embryonic rats were employed to create an injury model using 3 % sevoflurane. The sevoflurane-injured hippocampal neurons were treated with varying concentrations (10, 20, 40 and 80 μM/ml) of Rhodioloside to create different experimental groups: RHSD10+SEV, RHSD20+SEV, RHSD40+SEV, RHSD80+SEV, while untreated cells were considered as the Control group. Cell viability was identified using the CCK-8 assay. The CFSE assay was used to verify the promotion function of Rhodioloside on cell differentiation of neurons. FCM assay was employed to determine cell proliferation and apoptosis. Expression levels of apoptosisrelated factors, like Caspase-3, Bcl-2 and Bax were examined by RT-qPCR, while Western blot was used to measure phosphorylation of PKA.Results: Rhodioloside stimulated cell viability and prevented cell apoptosis in sevoflurane-injured hippocampal neurons in doses between 10-80 μM. The apoptosis-inhibitory effect of Rhodioloside was observed to be through cAMP/PKA pathway activation. Also, expression levels of Bcl-2, and PKA were enhanced and the level of Caspase-3 and Bax was reduced in a dose-dependent pattern. The PKA inhibitor reversed the above observation in the 40 μM Rhodioloside-treatment.Conclusion: Rhodioloside promoted cell viability and prevented apoptosis of primary hippocampal neurons injured by sevoflurane, through cAMP/PKA pathway activation. Inhibition of PKA network deteriorated the function of Rhodioloside by stimulating cell apoptosis. Our findings present a novel evidence that Rhodioloside could attenuate neurotoxicity of inhalational anesthetics. Keywords: Cell apoptosis, cAMP/PKA pathway, Hippocampal neurons, Rhodioloside, Sevoflurane

scholarly journals Endoplasmic reticulum stress regulates cell injury in lipopolysaccharide-induced nerve cells

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094976
Author(s):  
Min Li ◽  
Ying Zhang ◽  
Jixing Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Er Stress ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Injury ◽  
Cell Counting ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Stress Markers

Objective Sepsis-associated encephalopathy (SAE) is a common complication of sepsis, and excessive endoplasmic reticulum (ER) stress is closely correlated with the cell injury caused by sepsis. This study aimed to analyze the possible role of ER stress in SAE cell models. Methods PC12 and MES23.5 cells were treated with increasing concentrations of lipopolysaccharides (LPS). The Cell Counting Kit-8 assay was used to detect cell viability and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was performed to assess cell apoptosis. In addition, the protein expression levels of ER stress markers [GRP78, CHOP, inositol-requiring enzyme 1 (IRE1), and PKR-like ER kinase (PERK)] and apoptosis-related proteins (Bax, Bcl-2, caspase-3, and cleaved caspase-3) were analyzed using western blotting. Results LPS treatment activated ER stress markers in both the PC12 and MES23.5 cells. The overexpression of GRP78 significantly reduced cell viability and enhanced cell apoptosis in a time-dependent manner. An ER stress inhibitor, 4-PBA, significantly enhanced cell viability and inhibited the cell apoptosis induced by LPS. Therefore, an enhanced unfolded protein response (UPR) and UPR suppression may regulate cell apoptosis. Conclusions UPR was shown to be involved in regulating LPS-induced neuron injury. UPR could be a potential therapeutic target in SAE.

scholarly journals OS12.5 Small GTPase RHOE/RND3, a new critical regulator of NF-êB signaling in glioblastoma multiforme?

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii23-iii23
Author(s):  
B Liu ◽  
Q Chen
Keyword(s):  
Animal Model ◽  
Glioblastoma Multiforme ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Critical Role ◽  
Small Gtpase ◽  
Luciferase Assay ◽  
Tunel Staining ◽  
Apoptosis Resistance ◽  
Human Gbm

Abstract Background Abnormal activation of NF-κB signaling is a major mechanism of apoptosis resistance in glioblastoma multiforme (GBM). Therefore, better understanding of the regulation of NF-κB signaling has a significant impact for GBM therapy. Here, we uncovered a critical role of the small GTPase RND3 in regulating the p65 subunit of NF-κB and NF-κB signaling in GBM. MATERIALS AND METHODS Human GBM samples, GBM cells and a human orthotopic GBM-xenografted animal model were used. The mechanisms of RND3 in regulation of NF-κB signaling and GBM cell apoptosis were examined by luciferase assay, quantitative PCR, immunostaining, immunoblotting, immunofluorescence, co-immunoprecipitation, TUNEL staining, JC-1 analysis and flow cytometry. RESULTS Overexpression of RND3 led to reduced p65 activity in GBM cultured cells and a GBM animal model, indicating that the NF-κB pathway is negatively regulated by RND3 in GBM. Mechanistically, we found that RND3 bound p65 and promoted p65 ubiquitination, leading to decreased p65 protein levels. Furthermore, RND3 enhanced cleaved-caspase 3 levels and promoted apoptosis in GBM cells, and RND3 expression was positively correlated with cleaved-caspase 3 and IL-8 in human GBM samples. The effect of RND3 on promoting apoptosis disappeared when p65 ubiquitination was blocked by protease inhibitor carfilzomib or upon co-expression of ectopic p65. CONCLUSION RND3 binds p65 protein and promotes its ubiquitination, resulting in reduced p65 protein expression and inhibition of NF-κB signaling to induce GBM cell apoptosis.

Overexpression of miR-146a inhibits the apoptosis of hippocampal neurons of rats with cerebral hemorrhage by regulating autophagy

2020 ◽  
Vol 39 (9) ◽  
pp. 1178-1189
Author(s):  
S Huan ◽  
J Jin ◽  
C-x Shi ◽  
T Li ◽  
Z Dai ◽  
...  
Keyword(s):  
Western Blot ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Nuclear Factor Κb ◽  
Beclin 1 ◽  
Sprague Dawley ◽  
Related Factors ◽  
Expression Levels ◽  
Transmission Electron ◽  
Sprague Dawley Rats

In this study, to investigate the effect of overexpression of miR-146a on autophagy of hippocampal neurons in rats with intracerebral hemorrhage (ICH), 72 Sprague-Dawley rats were randomly divided into the sham, ICH, miR-146a agomir, and miR-146a agomir control groups. The ICH model was constructed by injection of collagenase VII. The apoptosis of hippocampal neurons was measured by TUNEL assay. The levels of LC3 and Beclin 1 were analyzed by immunohistochemistry. Mitochondrial autophagy was examined by transmission electron microscopy. The levels of LC3A, LC3B, Beclin 1, Bax, Bcl-2, and cleaved caspase 3 were examined by Western blot. Western blot was also used to evaluate the expression of nuclear factor κB signaling pathway-related factors. To examine the effect of autophagy inhibitor (3-methyladenine (3-MA)) on miR-146a-regulated apoptotic protein expression, 30 rats were further divided into the sham, ICH, miR-146a agomir, 3-MA, and miR-146a + 3-MA groups. The levels of Bax, Bcl-2, and cleaved caspase 3 were examined by Western blot. Compared with the sham group, the nerve function scores, brain water content, the percentage of apoptotic cells, and the expression levels of LC3, Beclin 1, Bax, cleaved caspase 3, and p-P65 in the hippocampus of rats in the ICH group were all significantly increased ( p < 0.05), whereas the expression levels of miR-146a, Bcl-2, and p-IκBα were markedly decreased ( p < 0.05). Mitochondrial autophagy was also evident. Furthermore, compared with the ICH group, the results of the abovementioned tests in the miR-146a agomir group were reversed. The overexpression of miR-146a inhibited the autophagy of hippocampal neurons in rats with ICH.

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

2021 ◽  
pp. 096032712110237
Author(s):  
Y-J Li ◽  
D-Z Zhang ◽  
Y Xi ◽  
C-A Wu
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Damage ◽  
Annexin V ◽  
Protective Effects ◽  
Gene And Protein Expression ◽  
And Oxidative Stress

Objective: To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Methods: Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. Results: DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. Conclusion: DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

Dexmedetomidine protects human renal tubular epithelial HK-2 cells against hypoxia/reoxygenation injury by inactivating endoplasmic reticulum stress pathway

2019 ◽  
Author(s):  
Mingyu Zhai ◽  
Mingming Han ◽  
Xiang Huang ◽  
Fang Kang ◽  
Chengwei Yang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blot ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Control Group ◽  
Sod Activity ◽  
Renal Tubular ◽  
Hypoxia Reoxygenation

Abstract Background: The study was aimed to explore the effects and potential mechanisms of Dexmedetomidine (Dex) on hypoxia/reoxygenation (H/R) injury in human renal tubular epithelial HK-2 cells. Methods: Human renal tubular epithelial HK-2 cells were divided into four groups: control group, Dex group, H/R group, and Dex + H/R group. After treatment, cell viability rate and cell apoptosis rate were measured by MTT assay and flow cytometry, respectively. Afterwards, the expressions of Hypoxia-inducible factor 1 (HIF-1α), glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), caspase-12 and cleaved caspase-3 were determined by western blot. Malondialdehyde (MDA) concentration and Superoxide Dismutase (SOD) activity were determined by assay kits. Results: Compared with control group, the cell viability rate was decreased and cell apoptotic was increased in H/R group. Besides, cell viability rate was increased, and cell apoptotic rate of HK-2 cells was decreased in Dex + H/R group, compared with H/R group. Western blot analysis showed that the expression of HIF-1α was up-regulated, and the expressions of GRP78, CHOP, capase-12 and cleaved caspase-3 were down-regulated in Dex + H/R group. In addition, the concentrations of MDA in Dex + H/R group and H/R group were 1.68 ± 0.22 nmol/mgprot and 0.85 ± 0.16 nmol/mgprot, which showed a 49.4% decrease in Dex + H/R group. However, after Dex treatment, the SOD activity was rose to 121 ± 11 U/L, which was more than twice larger than that in H/R group (57 ± 10 U/L). Conclusions: Dex could inhibit cell apoptosis by up-regulating the expression of HIF-1α, reducing endoplasmic reticulum stress and regulating oxidative stress, thus ameliorating the H/R injury.

Geniposide alleviates lipopolysaccharide (LPS)-induced inflammation by downregulation of miR-27a in rat pancreatic acinar cell AR42J

2019 ◽  
Vol 400 (8) ◽  
pp. 1059-1068 ◽  
Author(s):  
Xiaofen Zhang ◽  
Taishan Gao ◽  
Yanhua Wang
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Control Cell ◽  
Cell Counting ◽  
Pancreatic Acinar Cells ◽  
Protective Effects ◽  
Qrt Pcr ◽  
Ar42j Cells

Abstract Pancreatitis is a disease caused by inflammation of pancreatic acinar cells. Geniposide (GEN) possesses anti-inflammation activities. Hence, we investigated the effects of GEN on lipopolysaccharide (LPS)-stimulated AR42J cells. AR42J cells were stimulated by LPS and then treated with GEN and/or transfected with miR-27a mimic or negative control. Cell viability and cell apoptosis were detected using the Cell Counting Kit-8 and flow cytometry, respectively. All related proteins were measured by Western blot. The expression of miR-27a was detected by quantitative real time-polymerase chain reaction (qRT-PCR). Moreover, the expression of inflammatory cytokines interleukin-6 (IL-6) and monocyte chemoattractant protein (MCP)-1 was analyzed by qRT-PCR and Western blot. LPS significantly decreased cell viability, and enhanced cell apoptosis and IL-6, MCP-1 expression. Then GEN administration alleviated inflammatory injury by increasing cell viability, while reducing apoptosis, and IL-6 and MCP-1 expression. GEN downregulated miR-27a expression which was induced by LPS. Transfection with miR-27a mimic partially eliminated the protective effects of GEN. The phosphorylation of JNK and c-Jun was downregulated by GEN while upregulated by miR-27a overexpression. GEN alleviates LPS-induced AR42J cell injury as evidenced by promoting cell growth, and upregulation of IL-6 and MCP-1. This process might be modulated by down-regulating miR-27a and inactivation of JNK pathway.

scholarly journals MiR-140-3p inhibits the cell viability and promotes apoptosis of synovial fibroblasts in rheumatoid arthritis through targeting sirtuin 3

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Beibei Zu ◽  
Lin Liu ◽  
Jingya Wang ◽  
Meirong Li ◽  
Junxia Yang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Pearson Correlation ◽  
Fibrous Tissue ◽  
Synovial Fibroblasts ◽  
Cell Counting ◽  
Sirtuin 3 ◽  
Fibrous Tissues

Abstract Background Synovial fibroblasts (SFs) with the abnormal expressions of miRNAs are the key regulator in rheumatoid arthritis (RA). Low-expressed miR-140-3p was found in RA tissues. Therefore, we attempted to investigate the effect of miR-140-3p on SFs of RA. Methods RA and normal synovial fibrous tissue were gathered. The targets of miR-140-3p were found by bioinformatics and luciferase analysis. Correlation between the expressions of miR-140-3p with sirtuin 3 (SIRT3) was analyzed by Pearson correlation analysis. After transfection, cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry. The expressions of miR-140-3p, SIRT3, Ki67, Bcl-2, Bax, and cleaved Caspase-3 were detected by RT-qPCR or western blot. Results Low expression of miR-140-3p and high expression of SIRT3 were found in RA synovial fibrous tissues. SIRT3 was a target of miR-140-3p. SIRT3 expression was negatively correlated to the expression of miR-140-3p. MiR-140-3p mimic inhibited the MH7A cell viability and the expressions of SIRT3, Ki67, and Bcl-2 and promoted the cell apoptosis and the expressions of Bax and cleaved Caspase-3; miR-140-3p inhibitor showed an opposite effect to miR-140-3p mimic on MH7A cells. SIRT3 overexpression not only promoted the cell viability and inhibited cell apoptosis of MH7A cells but also reversed the effect of miR-140-3p mimic had on MH7A cells. Conclusions The results in this study revealed that miR-140-3p could inhibit cell viability and promote apoptosis of SFs in RA through targeting SIRT3.

scholarly journals Decitabine shows anti-acute myeloid leukemia potential via regulating the miR-212-5p/CCNT2 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 1013-1023
Author(s):  
Lina Xing ◽  
Jinhai Ren ◽  
Xiaonan Guo ◽  
Shukai Qiao ◽  
Tian Tian
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Myeloid Leukemia ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
Proliferation And Apoptosis ◽  
Polymerase Chain ◽  
The Relationship ◽  
Acute Myeloid

AbstractPrevious research has revealed the involvement of microRNA-212-5p (miR-212-5p) and cyclin T2 (CCNT2) in acute myeloid leukemia (AML). However, whether the miR-212-5p/CCNT2 axis is required for the function of decitabine in AML has not been well elucidated. Quantitative reverse transcription-polymerase chain reaction was used to examine enrichment of miR-212-5p. The relationship between CCNT2 and miR-212-5p was verified by the luciferase reporter assay. Cell apoptosis was evaluated by flow cytometry and western blot. CCK-8 assay was performed to determine cell viability. Decitabine significantly repressed cell viability, while promoted cell apoptosis. Meanwhile, the expression levels of cyclinD1, CDK4, and Bcl-2 were suppressed in cells with decitabine exposure, but Bax and caspase-3 expression levels were upregulated. Besides, miR-212-5p upregulation had the similar function with decitabine in AML cell proliferation and apoptosis. Subsequently, restoration of CCNT2 attenuated miR-212-5p overexpression-induced effects in Kasumi-1 and SKNO-1 cells. In addition, miR-212-5p depletion reversed decitabine-induced CCNT2 downregulation. The miR-212-5p/CCNT2 axis had an implication in the anti-leukemic effect of decitabine in AML.

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