MicroRNA-205-5p is upregulated in myelodysplastic syndromes and induces cell proliferation via PTEN suppression

Jang, Sook Jin; Choi, In Sun; Park, Geon; Moon, Dae Soo; Choi, Ji Seon; Nam, Mi Hyun; Yoon, Soo Young; Choi, Choong Hyeok; Kang, Seong‐Ho

doi:10.1016/j.leukres.2016.06.003

Cited by 15 publications

(8 citation statements)

References 26 publications

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“…For example, PTEN has been identified as a target gene of miR-21 in MDS and associated with TGFb signaling activation (48). miR-205-5p was upregulated in MDS cells and negatively regulated PTEN expression by directly targeting PTEN 3 0 -UTR (49). Overexpression of miR-17/92 has been found in lymphoid malignancies, and upregulation of miR-17/92 was closely correlated with expression of the proapoptotic factor Bim (50).…”

Section: Discussionmentioning

confidence: 99%

Morin Inhibits Proliferation and Induces Apoptosis by Modulating the miR-188-5p/PTEN/AKT Regulatory Pathway in CML Cells

Nie

Yang

Liu

et al. 2019

Molecular Cancer Therapeutics

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Increased activity of the PI3K/AKT/mTOR pathway has been observed in chronic myeloid leukemia (CML). Morin, a kind of flavonoid, exhibits a significant anticancer activity by suppressing the PI3K/AKT signaling pathway. However, the effect of morin on CML and its underlying mechanisms is poorly understood. Here, we found that morin dose dependently inhibited the proliferation of CML cell lines K562 and KCL22 and induced their apoptosis, with a significant increase in cell apoptosis upon exposure of cells to 50 mmol/L morin. Moreover, morin significantly reduced CML xenograft growth in nude mice. Mechanically, morin attenuated phosphorylated AKT level by upregulating PTEN expression, thus leading to the inhibition of AKT signaling. Knockdown of PTEN by its siRNA completely abrogated morin-induced cell apoptosis, indicating that PTEN mediates the inductive effect of morin on CML cell apoptosis. More importantly, we found that miR-188-5p was significantly upregulated in CML patients and CML cell lines. Treating CML cells with morin markedly downregulated the miR-188-5p expression level. Further, we demonstrated that miR-188-5p repressed PTEN expression by directly targeting its 3 0 -UTR. miR-188-5p downregulation induced by morin enhanced CML cell apoptosis by relieving miR-188-5p repression of PTEN expression. In summary, morin exerts significant anticancer efficacy in CML by regulating the miR-188-5p/PTEN axis and thus repressing the PI3K/AKT signaling.

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Section: Discussionmentioning

confidence: 99%

Morin Inhibits Proliferation and Induces Apoptosis by Modulating the miR-188-5p/PTEN/AKT Regulatory Pathway in CML Cells

Nie

Yang

Liu

et al. 2019

Molecular Cancer Therapeutics

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“…Increasing evidence have supported that miR-205-5p may play critical roles in cell proliferation, apoptosis, and extracellular matrix (ECM) deposition (22,23). And increased myofibroblasts and excessive ECM accumulation are the main characteristics of HS formation (24).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑205‑5p regulates extracellular matrix production in hyperplastic scars by targeting Smad2

Liu

et al. 2019

Exp Ther Med

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Hypertrophic scar (HS) formation is the result of poor skin-wound healing. At present, the pathogenesis of HS formation is largely unclear. Micro (miR)RNAs have important effects on a variety of biological and pathological processes. The role of miRNA in HS formation remains largely unclear. The present study aimed to investigate the role of miR-205-5p in HS, and explore the underlying molecular mechanism. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression of miR-205-5p in HS. Western blot assay and RT-qPCR were performed to assess the expression of associated proteins and genes, respectively. TargetScan was performed to predict the target gene of miR-205-5p, and the luciferase reporter assay was applied to verify the prediction. The function of miR-205-5p on cell proliferation was detected using Cell Counting Kit-8 assay, and cell apoptosis was detected via flow cytometry. miR-205-5p expression was decreased in HS tissues and human hypertrophic scar fibroblasts (hHSFs). Mothers against decapentaplegic homolog (Smad)2 was significantly increased in HS tissues and HSFs, and it was directly targeted by miR-205-5p. Restoration of miR-205-5p suppressed HSF cell proliferation and induced cell apoptosis. It was also demonstrated that RAC-Alpha Serine/Threonine-Protein Kinase (AKT) phosphorylation and the expression of α-smooth muscle actin, collagen I and collagen III were inhibited by miR-205-5p. In addition, Smad2 weakened the effects of miR-205-5p on HSFs. In conclusion, miR-205-5p exhibited an important role in HS by targeting smad2 and suppressing the AKT pathway. These findings provide a clearer understanding of the mechanism for HS that may be used to develop novel treatments for HS.

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“…In addition, increased expression levels of miRNA-205-5p are not associated with a decrease in the overall survival rate or with a certain prognostic group of MDS patients. This indicates that miRNA-205-5p is involved in the initiation, but not in the progression, of MDS [ 82 ]. Li et al .…”

Section: Micrornas In Mdsmentioning

confidence: 99%

MicroRNAs in the Myelodysplastic Syndrome

et al. 2021

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The myelodysplastic syndrome (MDS) holds a special place among blood cancers, as it represents a whole spectrum of hematological disorders with impaired differentiation of hematopoietic precursors, bone marrow dysplasia, genetic instability and is noted for an increased risk of acute myeloid leukemia. Both genetic and epigenetic factors, including microRNAs (miRNAs), are involved in MDS development. MicroRNAs are short non-coding RNAs that are important regulators of normal hematopoiesis, and abnormal changes in their expression levels can contribute to hematological tumor development. To assess the prognosis of the disease, an international assessment system taking into account a karyotype, the number of blast cells, and the degree of deficiency of different blood cell types is used. However, the overall survival and effectiveness of the therapy offered are not always consistent with predictions. The search for new biomarkers, followed by their integration into the existing prognostic system, will allow for personalized treatment to be performed with more precision. Additionally, this paper explains how miRNA expression levels correlate with the prognosis of overall survival and response to the therapy offered.

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MicroRNA-205-5p is upregulated in myelodysplastic syndromes and induces cell proliferation via PTEN suppression

Cited by 15 publications

References 26 publications

Morin Inhibits Proliferation and Induces Apoptosis by Modulating the miR-188-5p/PTEN/AKT Regulatory Pathway in CML Cells

Morin Inhibits Proliferation and Induces Apoptosis by Modulating the miR-188-5p/PTEN/AKT Regulatory Pathway in CML Cells

MicroRNA‑205‑5p regulates extracellular matrix production in hyperplastic scars by targeting Smad2

MicroRNAs in the Myelodysplastic Syndrome

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