miR-30a regulates γ-globin expression in erythoid precursors of intermedia thalassemia through targeting BCL11A

Gholampour, Mohammad Ali; Asadi, Marjan; Naderi, Mehran; Azarkeivan, Azita; Soleimani, Masoud; Atashi, Amir

doi:10.1007/s11033-020-05483-7

Cited by 17 publications

(17 citation statements)

References 33 publications

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“…For example, hsa‐miR‐15a and hsa‐miR‐16 target the MYB transcription factor to elevate γ‐globin expression 36,37 . Moreover, hsa‐miR‐210 , hsa‐miR‐30a , and hsa‐miR‐486‐3p regulate γ‐globin gene expression through the post‐transcriptional regulation of BCL11A expression 38‐40 . Importantly, let7 miRNAs have also been implicated in the developmental progression of fetal and adult human erythroblasts 41 .…”

Section: Introductionmentioning

confidence: 99%

“…36,37 Moreover, hsa-miR-210, hsa-miR-30a, and hsa-miR-486-3p regulate γ-globin gene expression through the posttranscriptional regulation of BCL11A expression. [38][39][40] Importantly, let7 miRNAs have also been implicated in the developmental progression of fetal and adult human erythroblasts. 41 In K-562 cells, hsa-miR-26b specifically activates the transcription factor GATA1 to increase the expression of γ-globin.…”

Section: Introductionmentioning

confidence: 99%

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Abnormal regulation of microRNAs and related genes in pediatric β‐thalassemia

Wang

Chen

et al. 2021

Clinical Laboratory Analysis

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Background MicroRNAs (miRNAs) participate in the reactivation of γ‐globin expression in β‐thalassemia. However, the miRNA transcriptional profiles of pediatric β‐thalassemia remain unclear. Accordingly, in this study, we assessed miRNA expression in pediatric patients with β‐thalassemia. Methods Differentially expressed miRNAs in pediatric patients with β‐thalassemia were determined using microRNA sequencing. Results Hsa‐miR‐483‐3p, hsa‐let‐7f‐1‐3p, hsa‐let‐7a‐3p, hsa‐miR‐543, hsa‐miR‐433‐3p, hsa‐miR‐4435, hsa‐miR‐329‐3p, hsa‐miR‐92b‐5p, hsa‐miR‐6747‐3p and hsa‐miR‐495‐3p were significantly upregulated, whereas hsa‐miR‐4508, hsa‐miR‐20a‐5p, hsa‐let‐7b‐5p, hsa‐miR‐93‐5p, hsa‐let‐7i‐5p, hsa‐miR‐6501‐5p, hsa‐miR‐221‐3p, hsa‐let‐7g‐5p, hsa‐miR‐106a‐5p, and hsa‐miR‐17‐5p were significantly downregulated in pediatric patients with β‐thalassemia. After integrating our data with a previously published dataset, we found that hsa‐let‐7b‐5p and hsa‐let‐7i‐5p expression levels were also lower in adolescent or adult patients with β‐thalassemia. The predicted target genes of hsa‐let‐7b‐5p and hsa‐let‐7i‐5p were associated with the transforming growth factor β receptor, phosphatidylinositol 3‐kinase/AKT, FoxO, Hippo, and mitogen‐activated protein kinase signaling pathways. We also identified 12 target genes of hsa‐let‐7a‐3p and hsa‐let‐7f‐1‐3p and 21 target genes of hsa‐let‐7a‐3p and hsa‐let‐7f‐1‐3p, which were differentially expressed in patients with β‐thalassemia. Finally, we found that hsa‐miR‐190‐5p and hsa‐miR‐1278‐5p may regulate hemoglobin switching by modulation of the B‐cell lymphoma/leukemia 11A gene. Conclusion The results of the study show that several microRNAs are dysregulated in pediatric β‐thalassemia. Further, the results also indicate toward a critical role of let7 miRNAs in the pathogenesis of pediatric β‐thalassemia, which needs to be investigated further.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Abnormal regulation of microRNAs and related genes in pediatric β‐thalassemia

Wang

Chen

et al. 2021

Clinical Laboratory Analysis

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“…It is mainly characterized by a chronic hemolytic anemia triggered by an incorrect hemoglobin synthesis linked with the absence or reduced production of β-globin chains. The insufficient synthesis of β-globin chains creates an imbalance between the α- and β-, δ- and γ-globin chains that lead to the precipitation of excess α-chains, thus aggravating an ineffective process of erythrocyte production within the bone marrow [ 154 , 155 , 156 ]. Thalassemia bone disease (TBD) is a common and severe complication of thalassemia.…”

Section: Other Bone Diseases and Mirnasmentioning

confidence: 99%

The Emerging Role of MicroRNAs in Bone Diseases and Their Therapeutic Potential

et al. 2021

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MicroRNAs (miRNAs) are a class of small (20–24 nucleotides), highly conserved, non-coding RNA molecules whose main function is the post-transcriptional regulation of gene expression through sequence-specific manners, such as mRNA degradation or translational repression. Since these key regulatory molecules are implicated in several biological processes, their altered expression affects the preservation of cellular homeostasis and leads to the development of a wide range of pathologies. Over the last few years, relevant investigations have elucidated that miRNAs participate in different stages of bone growth and development. Moreover, the abnormal expression of these RNA molecules in bone cells and tissues has been significantly associated with the progression of numerous bone diseases, including osteoporosis, osteosarcoma, osteonecrosis and bone metastasis, among others. In fact, miRNAs regulate multiple pathological mechanisms, including altering either osteogenic or osteoblast differentiation, metastasis, osteosarcoma cell proliferation, and bone loss. Therefore, in this present review, aiming to impulse the research arena of the biological implications of miRNA transcriptome in bone diseases and to explore their potentiality as a theragnostic target, we summarize the recent findings associated with the clinical significance of miRNAs in these ailments.

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“…MicroRNAs (miRNAs) are a category of conserved, small non-coding RNA molecules (21-25 nucleotides in length) 15,16 . Studies show that miRNAs play potential regulatory roles in β-thalassemia by interaction with BCL11A [17][18][19] . For instance, increased expression of miR-30a was associated with decreased BCL11A expression and elevated γ-globin and HbF levels in adult βthalassemia 17 .…”

Section: Introductionmentioning

confidence: 99%

“…Studies show that miRNAs play potential regulatory roles in β-thalassemia by interaction with BCL11A [17][18][19] . For instance, increased expression of miR-30a was associated with decreased BCL11A expression and elevated γ-globin and HbF levels in adult βthalassemia 17 . Another study showed that the coding mRNA sequence of BCL11A can be targeted by miR-210 and miR-486-3p in adult β-thalassemia 18,19 .…”

Section: Introductionmentioning

confidence: 99%

Down-Regulated hsa-miR-190b-5p is Correlated With BCL11A Expression in Pediatric β-Thalassemia

Chen

Wang

et al. 2021

Preprint

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Background: Transcription factor BCL11A is a key regulator of hemoglobin switching in adult β-thalassemia. Several microRNAs (miRNAs) involve in the pathology of β-thalassemia by regulations of BCL11A. However, the expressions and regulators of BCL11A in pediatric β-thalassemia were unclear. Methods: 18 pediatric β- thalassemia patients and 11 healthy controls were selected in this study. We applied reverse transcript quantitative real time PCR (RT-PCR) to analyze the expression levels of hsa-miR-190b-5p and γ-globin in pediatric β-thalassemia patients and luciferase activity assay to find out the direct regulations of BCL11A . Correlation between hsa-miR-190b-5p and biochemical indicators, BCL11A was assessed by the Pearson’s correlation test. Results: The expression levels of γ-globin in pediatric β-thalassemia patients were significantly increased. Moreover, the expression levels of hsa-miR-190b-5p were significantly down-regulated in pediatric β-thalassemia patients. Furthermore, hsa-miR-190b-5p was negatively correlated with BCL11A expression in pediatric β-thalassemia patients. Through luciferase activity assay, we found that hsa-miR-190b-5p was directly interacted with BCL11A 3’UTR 499-506 regions. Conclusion: Our results suggested that hsa-miR-190b-5p played key roles in regulating of BCL11A expression, which might provide novel therapies in pediatric patients with β-thalassemia .

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miR-30a regulates γ-globin expression in erythoid precursors of intermedia thalassemia through targeting BCL11A

Cited by 17 publications

References 33 publications

Abnormal regulation of microRNAs and related genes in pediatric β‐thalassemia

Abnormal regulation of microRNAs and related genes in pediatric β‐thalassemia

The Emerging Role of MicroRNAs in Bone Diseases and Their Therapeutic Potential

Down-Regulated hsa-miR-190b-5p is Correlated With BCL11A Expression in Pediatric β-Thalassemia

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