ArticleOncotarget2014
PLC-beta 1 regulates the expression of miR-210 during mithramycin-mediated erythroid differentiation in K562 cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- New Insights Into Pathophysiology of β-Thalassemia.Frontiers in medicine · 2022Pooled it
- Review
- PLCB4 upregulation is associated with unfavorable prognosis in pediatric acute myeloid leukemia.Oncology letters · 2019Article
- Diagnostic and prognostic value of mRNA expression of phospholipase C β family genes in hepatitis B virus‑associated hepatocellular carcinoma.Oncology reports · 2019Article
- MicroRNAs and Long Non-coding RNAs in Genetic Diseases.Molecular diagnosis & therapy · 2019Review
- Nuclear phospholipase C isoenzyme imbalance leads to pathologies in brain, hematologic, neuromuscular, and fertility disorders.Journal of lipid research · 2019Review
- BCL11A mRNA Targeting by miR-210: A Possible Network Regulating γ-Globin Gene Expression.International journal of molecular sciences · 2017Article
- miRNA143 Induces K562 Cell Apoptosis Through Downregulating BCR-ABL.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Up-regulated expression of phospholipase C, β1 is associated with tumor cell proliferation and poor prognosis in hepatocellular carcinoma.OncoTargets and therapy · 2016Article
- Article
- A novel DAG-dependent mechanism links PKCɑ and Cyclin B1 regulating cell cycle progression.Oncotarget · 2014Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PLC-beta 1 (PLCβ1) inhibits in human K562 cells erythroid differentiation induced by mithramycin (MTH) by targeting miR-210 expression. Inhibition of miR-210 affects the erythroid differentiation pathway and it occurs to a greater extent in MTH-treated cells. Overexpression of PLCβ1 suppresses the differentiation of K562 elicited by MTH as demonstrated by the absence of γ-globin expression. Inhibition of PLCβ1 expression is capable to promote the differentiation process leading to a recovery of γ-globin gene even in the absence of MTH. Our experimental evidences suggest that PLCβ1 signaling regulates erythropoiesis through miR-210. Indeed overexpression of PLCβ1 leads to a decrease of miR-210 expression after MTH treatment. Moreover miR-210 is up-regulated when PLCβ1 expression is down-regulated. When we silenced PKCα by RNAi technique, we found a decrease in miR-210 and γ-globin expression levels, which led to a severe slowdown of cell differentiation in K562 cells and these effects were the same encountered in cells overexpressing PLCβ1. Therefore we suggest a novel role for PLCβ1 in regulating miR-210 and our data hint at the fact that, in human K562 erythroleukemia cells, the modulation of PLCβ1 expression is able to exert an impairment of normal erythropoiesis as assessed by γ-globin expression.
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