Expressions of miR-181a and miR-20a in RPMI8226 cell line and their potential as biomarkers for multiple myeloma

Peng, Jing; Thakur, Asmitananda; Zhang, Shuo; Dong, Yuanfeng; Wang, Xiaoqin; Yuan, Ruili; Zhang, Kaige; Guo, Xuan

doi:10.1007/s13277-015-3600-2

Cited by 21 publications

(13 citation statements)

References 30 publications

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“…In the present study, the expression levels of miR-181a were significantly increased in BM samples from patients recently diagnosed with MM and in the MM RPMI8226 cell line compared with normal plasma cells, which was consistent with the results from previous studies (10,13,25). In the present study, upregulation of miR-181a was associated with disease stage, suggesting its potential contribution to the progression of MM.…”

Section: Discussionsupporting

confidence: 92%

“…miR-181a was the first miRNA reported to serve a regulatory role in B cell differentiation in the bone marrow (BM), and ectopic expression in hematopoietic stem/progenitor cells promoted a substantial increase in the generation of B cells, both in vitro and in vivo (12). Previous data have revealed that miR-181a is a biomarker of MM and regulates the progression of MM (13,14). In a number of different types of tumor, miR-181a was involved in the regulation of tumor proliferative, migratory and invasive abilities, thereby highlighting its potential as a prognostic factor and therapeutic target (15).…”

Section: Introductionmentioning

confidence: 99%

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MiR‑181a functions as an oncogene by regulating CCND1 in multiple myeloma

et al. 2020

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MicroRNA-181a (miR-181a) has been demonstrated to be upregulated in patients with multiple myeloma (MM). In several studies, miR-181a has been demonstrated to be significantly overexpressed in MM; however, its potential role in development and progression of MM remains unknown. In the present study, the functions of miR-181a and the potential underlying molecular mechanisms in the pathogenesis of MM were examined. Increased expression of miR-181a was observed in bone marrow samples from patients with MM and the MM RPMI8226 cell line. The role of miR-181a was examined and it was demonstrated that it participated in the proliferation and migration processes of the MM cell line. Furthermore, it was demonstrated that the downregulation of miR-181a inhibited the expression of CCND1, a cell cycle regulatory gene, and caused cell cycle arrest in MM cells. The results of the present study suggested that miR-181a functions as an onco-miRNA in MM, which serves regulatory roles by upregulating expression of CCND1 and may therefore serve as a potential target in patients with MM.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

MiR‑181a functions as an oncogene by regulating CCND1 in multiple myeloma

et al. 2020

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“…Several members of the miR-17-92 cluster regulate cell proliferation. For example, miR-17-5p promoted cell proliferation in gastric 39 and colorectal cancer cell lines 40 , and miR-20a promoted cell proliferation in human lung cancer 41 and multiple myeloma 42 . In the present study, we demonstrated that the miR-17-92 cluster promotes chicken cell proliferation through its two members, miR-17-5p and miR-20a (Fig.…”

Section: Discussionmentioning

confidence: 99%

MiR-17-5p and miR-20a promote chicken cell proliferation at least in part by upregulation of c-Myc via MAP3K2 targeting

Zhang

Qiao

et al. 2017

Sci Rep

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The miR-17-92 cluster has been well studied in mammals but less extensively studied in birds. Here, we demonstrated that miR-17-92 cluster overexpression promoted the proliferation of DF1 cells and immortalized chicken preadipocytes (ICPA-1), and miR-17-5p and miR-20a, members of the miR-17-92 cluster, targeted MAP3K2. Further analysis showed that MAP3K2 overexpression reduced the proliferation of DF1 and ICPA-1 cells and attenuated the promotive effect of the miR-17-92 cluster on cell proliferation. Downstream gene expression analysis of the MAPK signalling pathway showed that MAP3K2 overexpression decreased c-Myc expression; in contrast, MAP3K2 knockdown using RNA interference and miR-17-92 cluster overexpression increased c-Myc expression. Furthermore, c-Myc overexpression promoted miR-17-92 cluster expression and DF1 cell proliferation. Taken together, these data indicated that miR-17-92 promotes chicken cell proliferation at least in part by the upregulation of c-Myc via targeting MAP3K2, and the miR-17-92 cluster, c-Myc and E2F1 form a complex regulatory network in chicken cell proliferation.

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“…miR-20a has an important in various human cancers, including gastric cancer (15), colorectal cancer (16), non-small cell lung cancer (17) and cervical cancer (18). Importantly, significant expression of miR-20 has been found in myeloma (19,20). Several studies have suggested that the dysregulation of miRNAs initiates the activation of the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway,…”

Section: Introductionmentioning

confidence: 99%

Effects of microRNA‑20a on the proliferation, migration and apoptosis of multiple myeloma via the PTEN/PI3K/AKT signaling pathway

2018

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Multiple myeloma (MM) is a heterogeneous disease with a poor prognosis. Circulating microRNAs (miRNAs) have shown potential as non-invasive prognostic biomarkers for heterogeneous diseases. miR-20a has been shown involved in various human cancers, and the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B (PTEN/P13K/Akt) signaling pathway plays a key role in cell proliferation, migration and apoptosis. Here, we investigated the effect of miR-20a on the PTEN/PI3K/Akt signaling pathway during MM cell proliferation, migration and apoptosis. Reverse transcription quantitative polymerase chain reaction was applied to detect miR-20a expression in plasma from 30 MM patients and MM cell lines. CCK-8 assays, Transwell assays, Annexin V/PI double-staining and western blotting were performed to examine the protein expressions of PTEN, PI3K and Akt during cellullar proliferation, migration, cycling, and apoptosis. Significant upregulation of miR-20a and deregulation of PTEN were observed in MM cells. We also identified PTEN as a downstream target gene of miR-20a, which bound to the 3'-untranslated region of PTEN. Overexpression of miR-20a was associated with decreased PTEN expression, and treatment with miR-20a inhibitors decreased cell proliferation, migration and clonogenicity and reduced the protein expressions of PI3K and p-Akt but increased PTEN protein expression compared with blank and negative control groups. Taken together, these results showed that inhibition of miR-20a suppresses MM progression by modulating the PTEN/PI3K/Akt signaling pathway. These findings suggest that miR-20a may be a novel molecular therapeutic target for the treatment of MM.

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Expressions of miR-181a and miR-20a in RPMI8226 cell line and their potential as biomarkers for multiple myeloma

Cited by 21 publications

References 30 publications

MiR‑181a functions as an oncogene by regulating CCND1 in multiple myeloma

MiR‑181a functions as an oncogene by regulating CCND1 in multiple myeloma

MiR-17-5p and miR-20a promote chicken cell proliferation at least in part by upregulation of c-Myc via MAP3K2 targeting

Effects of microRNA‑20a on the proliferation, migration and apoptosis of multiple myeloma via the PTEN/PI3K/AKT signaling pathway

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