MiR-645 regulates the proliferation and apoptosis of diffuse large B-cell lymphoma by targeting DACH1
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RESEARCH ARTICLE
MiR‑645 regulates the proliferation and apoptosis of diffuse large B‑cell lymphoma by targeting DACH1 Ruihuan Wang1 · Jie Shen1 · Na Su2 · Qing Wang1 · Minjuan Zhang1 · Chunyan Liu1 Received: 13 September 2019 / Accepted: 2 January 2020 © Japan Human Cell Society and Springer Japan KK, part of Springer Nature 2020
Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of malignant non-Hodgkin lymphoma cases. An increasing body of evidence has indicated the critical roles of microRNAs (miRNAs) in regulating the progression of DLBCL. In this study, we found that miR-645 was up-regulated in DLBCL tissues and cell lines. Down-regulation of miR-645 significantly inhibited the proliferation, cell cycle progression and promoted the apoptosis of DLBCL cells. Experimental study identified Dachshund family transcription factor 1 (DACH1) as a target of miR-645. MiR-645 bound the 3′-untranslated region of DACH1 and reduced the expression of DACH1 in DLBCL cells. Decreased expression of DACH1 was inversely correlated with that of miR-645 in DLBCL tissues. The promoting effect of miR-645 on the proliferation of DLBCL cells was attenuated with the overexpression of DACH1. These results demonstrated the novel mechanism of miR-645 in DLBCL, which indicated miR-645 as a potential target for the diagnosis and prognostics of DLBCL. Keywords miR-645 · DLBCL · DACH1
Introduction Diffuse large-B cell lymphoma (DLBCL) is the most common type of non-Hodgkin’s lymphoma based on the morphological and prognostic features [1, 2]. With the progress in the therapy for DLBCL, the clinical outcome of DLBCL patients has been greatly improved; however, the morbidity rate still increased in recent years. Therefore, it is quite necessary to understand the molecular mechanisms that are responsible for the development of DLBCL. MicroRNA (miRNAs) are a class of small, non-coding, single-stranded RNA transcripts without protein-coding capacity [1, 2]. It has been well documented that miRNAs act as negative regulators of gene expression via binding Electronic supplementary material The online version of this article (https://doi.org/10.1007/s13577-020-00321-1) contains supplementary material, which is available to authorized users. * Ruihuan Wang [email protected] 1
The Second Hematology Department, Cangzhou Central Hospital, No. 16 Xinhua West Street, Cangzhou 061001, Hebei, China
The CDC of Xinhua District, Cangzhou 061000, Hebei, China
2
the 3′-untranslated region (UTR) of target genes, resulting in the degradation or translation inhibition of mRNAs [3–6]. Increasing evidence has indicated the implication of miRNAs in the progression of human cancers [7–11]. Aberrant expression of miRNAs modulated the proliferation, differentiation and migration of cancer cells. For example, recent study showed that decreased expression of miR-101 was correlated with the prognosis of DLBCL. Up-regulation of miR-101 suppressed DLBCL cell proliferation through regulating the expression of MAPK kinase 1 [12]. Overe
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