The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

Wang, Yan; Guo, Hua; Suo, Feng; Han, Chunling; Zheng, Hua; Chen, Tong

doi:10.3892/ol.2016.5395

Cited by 15 publications

(14 citation statements)

References 21 publications

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“…Has-mir-130a was involved in the megakaryocytic differentiation and erythropoiesis, and its expression was also related to the differentiation patterns in AML [12]. Has-mir-146a was a regulator of apoptosis [13], and its expression was associated with patient prognosis of AML. The increase of has-mir-146a can enhance the sensitivity of leukemic blast cells to cytotoxic drugs [14].…”

Section: Discussionmentioning

confidence: 98%

Transcriptome analysis identifies key regulators and networks in Acute myeloid leukemia

Luo

et al. 2019

Hematology

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Objectives: Acute myeloid leukemia (AML) is a heterogeneous and highly recurrent hematological malignancy. Studies have shown an association between microRNAs and drive genes in AMLs. However, the regulatory roles of miRNAs in AML and how they act on downstream targets and the signaling pathway has been little studied. Methods: As to understand the mechanism of mRNA-miRNA interaction in the blood malignancy from a large scale of transcriptomic sequencing studies, we applied a comprehensive miRNA-mRNA association, co-expression gene network and ingenuity pathway analysis using TCGA AML datasets. Results: Our results showed that his-mir-335 was a critical regulatory of homeobox A gene family. PBX3, KAT6A, MEIS1, and COMMD3-BMI1 were predicted as top transcription regulators in the regulatory network of the HOXA family. The most significantly enriched functions were cell growth, proliferation, and survival in the mRNA-miRNA network. Conclusion: Our work revealed that regulation of the HOXA gene family and its regulation played an important role in the development of AML.

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Section: Discussionmentioning

confidence: 98%

Transcriptome analysis identifies key regulators and networks in Acute myeloid leukemia

Luo

et al. 2019

Hematology

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“…In particular, an overexpression of the mir-146 gene was observed. miR-146 can regulate the expression of the apoptosis factor STAT1, and the anti-apoptosis factor Bcl-xL, thus promoting the apoptosis of ALL cells [44]. Furthermore, tumour protein P63 gene (TP63 gene) was also upregulated in E/R KO clones as compared with control clones.…”

Section: Discussionmentioning

confidence: 99%

ETV6/RUNX1 Fusion Gene Abrogation Decreases the Oncogenicity of Tumour Cells in a Preclinical Model of Acute Lymphoblastic Leukaemia

Montaño

Ordóñez

Alonso-Pérez

et al. 2020

Cells

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Background: The t(12;21)(p13;q22), which fuses ETV6 and RUNX1 genes, is the most common genetic abnormality in children with B-cell precursor acute lymphoblastic leukaemia. The implication of the fusion protein in leukemogenesis seems to be clear. However, its role in the maintenance of the disease continues to be controversial. Methods: Generation of an in vitro ETV6/RUNX1 knock out model using the CRISPR/Cas9 gene editing system. Functional characterization by RNA sequencing, proliferation assays, apoptosis and pharmacologic studies, and generation of edited-cell xenograft model. Results: The expression of ETV6/RUNX1 fusion gene was completely eliminated, thus generating a powerful model on which to study the role of the fusion gene in leukemic cells. The loss of fusion gene expression led to the deregulation of biological processes affecting survival such as apoptosis resistance and cell proliferation capacity. Tumour cells showed higher levels of apoptosis, lower proliferation rate and a greater sensitivity to PI3K inhibitors in vitro along as a decrease in tumour growth in xenografts models after ETV6/RUNX1 fusion gene abrogation. Conclusions: ETV6/RUNX1 fusion protein seems to play an important role in the maintenance of the leukemic phenotype and could thus become a potential therapeutic target.

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“…24,25 Through our literature review, we found some influential review focused on miRNAs in childhood ALL have mentioned miR-100, miR-210, and miR-146a in common. 8,9 In the present study, we focused on genetic variants of miR-100, miR-146a, and miR-210, which were all demonstrated to be participate in carcinogenesis of ALL, 13,14,16 and investigated their association with susceptibility of childhood ALL. Among them, rs7395206 have never been reported in other studies while rs543412 and rs2910164 has not been detected in Chinese childhood ALL groups.…”

Section: Discussionmentioning

confidence: 99%

A genetic variant in miR‐100 is a protective factor of childhood acute lymphoblastic leukemia

Xue

Yang

et al. 2019

Cancer Medicine

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Background In the past decade, miR‐100, miR‐146a, and miR‐210 were reported to be dysregulated in childhood acute lymphoblastic leukemia (ALL). However, effects of genetic variants in these three microRNAs have not been investigated in Chinese population. Methods In this study, we conducted a case‐control study to evaluate the relationship between genetic variants in miR‐100, miR‐146a, and miR‐210 and the risk of childhood ALL in Chinese population. Subsequently, plasma expression level of miR‐100 was also detected. Result We found that subjects carrying mutant homozygous TT genotype of miR‐100 rs543412 had a statistically significantly decreased risk of childhood ALL (adjusted odds ratio [OR] = 0.73, 95% confidence interval [CI] = 0.55‐0.97, P = 0.029). This protective effect was also observed among subjects whose parents were ever drinkers (adjusted OR = 0.53, 95% CI = 0.29‐0.94), or whose living house were ever painted (adjusted OR = 0.57, 95% CI = 0.34‐0.94). Besides, rs543412 variant homozygous TT had a significantly protective role in patients with childhood B‐ALL. Finally, we found that expression level of miR‐100 in plasma of childhood ALL cases was significantly higher than that of noncancer controls. Conclusion Our study suggested that there was significant association between the polymorphisms in miR‐100 (rs543412) and decreased susceptibility to childhood ALL.

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The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

Cited by 15 publications

References 21 publications

Transcriptome analysis identifies key regulators and networks in Acute myeloid leukemia

Transcriptome analysis identifies key regulators and networks in Acute myeloid leukemia

ETV6/RUNX1 Fusion Gene Abrogation Decreases the Oncogenicity of Tumour Cells in a Preclinical Model of Acute Lymphoblastic Leukaemia

A genetic variant in miR‐100 is a protective factor of childhood acute lymphoblastic leukemia

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