Downregulated miR‑130a enhances the sensitivity of acute myeloid leukemia cells to Adriamycin

Liu, Huimin; Liu, Min; Zhang, Jiangzhao; Liang, Yan

doi:10.3892/mmr.2020.11375

Cited by 4 publications

(4 citation statements)

References 36 publications

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“…In general, this microRNA has a dual role in biological processes. Due to its cellular functions, miR-130a expression is dysregulated in a variety of pathologies, including oral squamous cell carcinoma 17 , ovarian epithelial cell carcinoma, thyroid eye disease 18 , cervical cancer 19 , and acute myeloid leukemia 20 . It was also shown that upregulated miR-130a reduces intracellular ATP levels in the pancreatic beta cell 21 .…”

Section: Discussionmentioning

confidence: 99%

Analysis of serum circulating MicroRNAs level in Malaysian patients with gestational diabetes mellitus

pour

Zain

Vazifehmand

et al. 2022

Sci Rep

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Gestational diabetes mellitus (GDM) is a severe global issue that requires immediate attention. MicroRNA expression abnormalities are possibly disease-specific and may contribute to GDM pathological processes. To date, there is limited data on miRNA profiling in GDM, especially that involves a longitudinal study. Here, we performed miRNA expression profiling in the entire duration of pregnancy (during pregnancy until parturition and postpartum) using a miRNA- polymerase chain reaction array (miRNA-PCRArray) and in-silico analysis to identify unique miRNAs expression and their anticipated target genes in Malay maternal serum. MiRNA expression levels and their unique potential as biomarkers were explored in this work. In GDM patients, the expression levels of hsa-miR-193a, hsa-miR-21, hsa-miR-23a, and hsa-miR-361 were significantly increased, but miR-130a was significantly downregulated. The area under the curve (AUC) and receiver operating characteristic (ROC) curve study demonstrated that hsa-miR-193a (AUC = 0.89060 ± 04,470, P = 0.0001), hsa-miR-21 (AUC = 0.89500 ± 04,411, P = 0.0001), and miR-130a (AUC = 0.6939 ± 0.05845, P = 0.0025) had potential biomarker features in GDM. In-silico analysis also revealed that KLF (Kruppel-Like family of transcription factor), ZNF25 (Zinc finger protein 25), AFF4 (ALF transcription elongation factor 4), C1orf143 (long intergenic non-protein coding RNA 2869), SRSF2 (serine and arginine rich splicing factor 2), and ZNF655 (Zinc finger protein 655) were prominent genes targeted by the common nodes of miR23a, miR130, miR193a, miR21, and miR361.Our findings suggest that circulating microRNAs in the first trimester has the potential for GDM screening in the Malay population.

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Section: Discussionmentioning

confidence: 99%

Analysis of serum circulating MicroRNAs level in Malaysian patients with gestational diabetes mellitus

pour

Zain

Vazifehmand

et al. 2022

Sci Rep

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“…AML involves malignant cloning of blood stem cells and is frequently associated with multiple genetic alterations [ 16 ]. AML is characterized by abnormal proliferation and differentiation of immature myeloid cells and impaired apoptosis, leading to suppression of the hematopoietic system, the complex pathogenesis of which has not been fully elucidated [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Action of Decitabine in the Treatment of Acute Myeloid Leukemia by Regulating LINC00599

Fan

Jin

Wang

2023

Analytical Cellular Pathology

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Objective. Acute myeloid leukemia (AML) is a heterogeneous malignancy with a low long-term survival rate. The aim of this study was to investigate the effects of decitabine (DAC) treatment cell proliferation and apoptosis in AML and role of the expression of LINC00599 and, consequently, miR-135a-5p. Materials and Methods. Human promyelocytic leukemia cells (HL-60) and human acute lymphatic leukemia (CCRF-CEM) cells were treated with various concentrations of DAC. Cell proliferation in each group was detected using the cell counting kit 8. For each group, apoptosis and reactive oxygen species (ROS) levels were detected using flow cytometry. Reverse transcription polymerase chain reaction (RT-PCR) was performed to examine the expression of lncRNA LINC00599. The expression of apoptosis-related proteins was analyzed using western blotting. The regulatory relationship between miR-135a-5p and LINC00599 was verified by constructing miR-135a-5p mimics, miR-135a-5p inhibit, wild type LINC00599 3 ′ -untranslated region (UTR), and mutant LINC00599 3 ′ -UTR. Ki-67 expression in the tumor tissues of nude mice was detected using immunofluorescent assays. Results. Both DAC and LINC00599 Inhibit groups were able to significantly reduce the proliferation of HL60 and CCRF-CEM cells, increase apoptosis, upregulate the expression of Bad, cleaved caspase-3, and miR-135a-5p, downregulate the expression of Bcl-2, and elevate ROS levels in cells, with these effects being more pronounced after combined treatment with DAC and LINC00599 Inhibit. In comparison to mimic NC, the miR-135a-5p mimic group significantly decreased the relative fluorescence activity ratio of LINC00599 3 ′ -UTR wild-type CCRF-CEM cells. The LINC00599 Inhibit and miR-135a-5p mimic groups exhibited substantially reduced proliferation of HL60 and CCRF-CEM cells, increased apoptosis, upregulated Bad, cleaved caspase-3, and miR-135a-5p expression, along with downregulated Bcl-2 and LINC00599 expression and increased ROS levels in cells; these effects were more pronounced after LINC00599 Inhibit was combined with miR-135a-5p mimics. In vivo experiments revealed that both DAC and LINC00599 Inhibit were able to considerably reduce the long diameter, short meridian, volume, and mass of tumors, increase miR-135a-5p expression, and decrease LINC00599 and ki-67 expression in tumor tissues of nude mice. This effect was more pronounced when the DAC and LINC00599 Inhibit were used in combination. Conclusion. DAC regulates the expression of miR-135a-5p by regulating the expression of LINC00599, which in turn affects cell proliferation, apoptosis, and tumor proliferation. Our findings provide a theoretical basis for improving the clinical outcome of AML.

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“…Under hypoxia, hypoxia‐inducible factor‐1α can activate EMT in leukemia stem cells, increasing the resistance of AML cells to cytarabine 22 . MicroRNA‐130a can increase AML cell chemoresistance by EMT 23 . However, no attention has been paid to the potential of the AML‐MSC‐induced EMT program in AML.…”

Section: Introductionmentioning

confidence: 99%

“… 22 MicroRNA‐130a can increase AML cell chemoresistance by EMT. 23 However, no attention has been paid to the potential of the AML‐MSC‐induced EMT program in AML.…”

Section: Introductionmentioning

confidence: 99%

Acute myeloid leukemia (AML)‐derived mesenchymal stem cells induce chemoresistance and epithelial–mesenchymal transition‐like program in AML through IL‐6/JAK2/STAT3 signaling

Dong

Zhang

et al. 2023

Cancer Science

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Acute myeloid leukemia (AML) has a high rate of treatment failure due to increased prevalence of therapy resistance. Mesenchymal stem cells (MSCs) in the leukemia microenvironment contribute to chemoresistance in AML, but the specific mechanism remains unclear. The critical role of the epithelial-mesenchymal transition (EMT)-like profile in AML chemoresistance has been gradually recognized. However, there is no research to suggest that the AML-derived bone marrow mesenchymal stem cells

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Downregulated miR‑130a enhances the sensitivity of acute myeloid leukemia cells to Adriamycin

Cited by 4 publications

References 36 publications

Analysis of serum circulating MicroRNAs level in Malaysian patients with gestational diabetes mellitus

Analysis of serum circulating MicroRNAs level in Malaysian patients with gestational diabetes mellitus

Mechanism of Action of Decitabine in the Treatment of Acute Myeloid Leukemia by Regulating LINC00599

Acute myeloid leukemia (AML)‐derived mesenchymal stem cells induce chemoresistance and epithelial–mesenchymal transition‐like program in AML through IL‐6/JAK2/STAT3 signaling

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