MicroRNA-183 promotes cell proliferation via regulating programmed cell death 6 in pediatric acute myeloid leukemia

Wang, Xiang; Zuo, Dongjian; Yuan, Yufang; Yang, Xiaochun; Zhang, Hong; Zhang, Rongrong

doi:10.1007/s00432-016-2277-2

Cited by 30 publications

(20 citation statements)

References 28 publications

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“…Other studies have shown that expression of GSK3β can inhibit the expression of miR-183 through the β-Catenin/TCF/LEF-1 pathway in human gastric cancer cells, while β-Catenin/TCF/ LEF-1 binds to the promoter of miR-183 and thereby activates the transcription of miR-183 [8]. While in non-small cell lung cancer, they found that TFAP2C blocked AKAP12-mediated cyclin D1 inhibition by inducing the overexpression of miR-183, which shows that TFAP2C is one of the upstream regulators of miR-183 [9]. In breast cancer, the transcription of miR-183 was regulated by ZEB1 and HSF2, HSF2 can upregulate miR-183 expression [10].…”

Section: Regulation Of Mir-183 Expressionmentioning

confidence: 98%

MicroRNA-183 in Cancer Progression

Cao¹,

Di²,

Liang³

et al. 2020

J. Cancer

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MicroRNA -183(miR-183) is abnormally expressed in many kinds of tumors. It participates in the initiation and development of tumors. There are many pathways regulate the expression of miR-183. The action mechanism of miR-183 in cancer is very extensive, and contradictory conclusions are often drawn. It was upregulated in 18 kinds of cancer, downregulated in 6 kinds of cancer. In addition, there are seven types of cancer, both upregulated and downregulated reports can be found. Evidence showed that miR-183 can not only directly play the role of oncogene or antioncogene, but also regulate the expression of other oncogene or antioncogene in different cancer types. In this review, we discuss the regulator of miR-183 and summarized the expression of miR-183 in different cancers. We also counted the target genes of miR-183 and the functional roles they play. Furthermore, we focused on the roles of miR-183 in cell migration, cell invasion, epithelial-mesenchymal transition (EMT) and microangiogenesis, which play the most important roles in cancer processes. It sheds light on the likely reasons why miR-183 plays different roles in various cancers. In addition, miR-183 and its downstream effectors have the potential to be promising prognostic markers and therapeutic targets in cancer.

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Section: Regulation Of Mir-183 Expressionmentioning

confidence: 98%

MicroRNA-183 in Cancer Progression

Cao¹,

Di²,

Liang³

et al. 2020

J. Cancer

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“…Increasing evidence has demonstrated that miRNAs participate in various fundamental biological and pathological processes, such as cell differentiation, proliferation, apoptosis, as well as autophagy, indicating their important regulatory roles during carcinogenesis and chemoresistance [21]. It is well documented that dysregulation of miRNAs contributes to a variety of human disease, including AML [22], [23]. In view of the significance of autophagy in the chemoresistance of tumors and the regulatory role of miRNAs in autophagy, better understanding the role of miRNA-regulated autophagy during chemotherapy in AML might contribute to clarifying its mechanism of chemoresistance.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-142-3p Improves Drug Sensitivity of Acute Myelogenous Leukemia through Reducing P-Glycoprotein and Repressing Autophagy by Targeting HMGB1

Zhang

Liu

2017

Translational Oncology

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miR-142-3p was reported to be downregulated in acute myelogenous leukemia (AML) and acted as a novel diagnostic marker. However, the regulatory effect of miR-142-3p on drug resistance of AML cells and its underlying mechanism have not been elucidated. Here, we found that miR-142-3p was significantly downregulated and high mobility group box 1 (HMGB1) was dramatically upregulated in AML samples and cells, as well as drug-resistant AML cells. P-gp level and autophagy were markedly enhanced in HL-60/ADR and HL-60/ATRA cells. miR-142-3p overexpression improved drug sensitivity of AML cells by inhibiting cell viability and promoting apoptosis, and inhibited P-gp level and autophagy in drug-resistant AML cells, whereas HMGB1 overexpression obviously reversed these effect. HMGB1 was demonstrated to be a target of miR-142-3p, and miR-142-3p negatively regulated HMGB1 expression. In conclusion, our study elucidated that upregulation of miR-142-3p improves drug sensitivity of AML through reducing P-glycoprotein and repressing autophagy by targeting HMGB1, contributing to better understanding the molecular mechanism of drug resistance in AML.

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“…Ke et al showed that miR-192 suppressed the proliferation, cell cycle transition of AML cells by targeting CCNT2 (24). In addition, Wang et al demonstrated that miR-183 enhanced the proliferation of pediatric AML cells by targeting programmed cell death 6 (25). miR-135a has been shown to aberrantly expressed in several cancer, including non-small cell lung cancer (26), thyroid carcinoma (27), glioblastoma (28), pancreatic cancer (29), hepatocellular carcinoma (30) and gastric cancer (31).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR‑135a predicts poor prognosis in acute myeloid leukemia and regulates leukemia progression via modulating HOXA10 expression

Wen

2018

Mol Med Report

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MicroRNA‑135a (miR‑135a) has been shown to exert important roles in various human cancer types, such as glioblastoma, thyroid carcinoma and renal carcinoma. However, the function of miR‑135a in acute myeloid leukemia (AML) remains largely unknown. In the present study, it was demonstrated that miR‑135a expression was significantly downregulated in AML cells compared with normal control cells. Furthermore, the downregulation of miR‑135a in patients with AML predicted poor prognosis. Through functional experiments, overexpression of miR‑135a was demonstrated to significantly inhibit the proliferation and cell cycle of AML cells, while it promoted cellular apoptosis. miR‑135a directly targeted HOXA10 in AML cells. miR‑135a overexpression significantly suppressed the mRNA and protein levels of HOXA10 in AML cells. Moreover, there was an inverse association between miR‑135a expression and HOXA10 level in AML samples. Additionally, by ectopic expression of HOXA10, restoration of HOXA10 significantly abolished the effects of miR‑135a overexpression on AML cell proliferation, cell cycle and apoptosis. In conclusion, the present study demonstrated that miR‑135a serves as a tumor suppressor in AML by targeting HOXA10, and miR‑135a may be a promising prognostic biomarker for AML patients.

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MicroRNA-183 promotes cell proliferation via regulating programmed cell death 6 in pediatric acute myeloid leukemia

Abstract: Combined serum miR-183 and PDCD6 mRNA may serve as a novel prognostic biomarker for pediatric AML. Interestingly, miR-183 may function as an oncogene and may enhance cell proliferation by targeting PDCD6, implying a potential therapeutic target for this malignancy.

Cited by 30 publications

References 28 publications

MicroRNA-183 in Cancer Progression

MicroRNA-183 in Cancer Progression

Upregulation of miR-142-3p Improves Drug Sensitivity of Acute Myelogenous Leukemia through Reducing P-Glycoprotein and Repressing Autophagy by Targeting HMGB1

Downregulation of miR‑135a predicts poor prognosis in acute myeloid leukemia and regulates leukemia progression via modulating HOXA10 expression

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