MicroRNA-124 suppresses growth of human hepatocellular carcinoma by targeting STAT3

Lu, Yanxin; Yue, Xupeng; Cui, Yuanyuan; Zhang, Jufeng; Wang, Kewei

doi:10.1016/j.bbrc.2013.10.157

Cited by 68 publications

(61 citation statements)

References 26 publications

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“…This miRNA represses cell proliferation, cell survival, migration, and invasion by targeting cancer relevant genes such as RelA/p65, STAT3, EZH2, and Slug (Liang et al, 2013;Lu et al, 2013;Ning et al, 2014;Xie et al, 2014). Indeed, miR-124 expression is attenuated in different types of tumors, including hematological malignancies (Wong et al, 2011).…”

Section: Introductionmentioning

confidence: 98%

MicroRNA-124 regulates glucocorticoid sensitivity by targeting phosphodiesterase 4B in diffuse large B cell lymphoma

Kim

Jeong

Nam

et al. 2015

Gene

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Section: Introductionmentioning

confidence: 98%

MicroRNA-124 regulates glucocorticoid sensitivity by targeting phosphodiesterase 4B in diffuse large B cell lymphoma

Kim

Jeong

Nam

et al. 2015

Gene

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“…[10][11][12] Recently, the miR-124 promoter was found to be hypermethylated in hematological malignancies, including B-cell lymphomas, in association reduced expression. 13 Mechanistically, the role of miR-124 in liver cancer was associated with p65 targeting.…”

mentioning

confidence: 99%

MicroRNA-124 links p53 to the NF-κB pathway in B-cell lymphomas

et al. 2015

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The contribution of microRNAs to lymphoma biology is not fully understood. In particular, it remains untested whether microRNA dysregulation could contribute to the emergence of the aggressive subset of B-cell lymphomas that coexpress MYC and BCL2. Here, we identify microRNA-124 (miR-124) as a negative regulator of MYC and BCL2 expression in B-cell lymphomas. Concordantly, stable or transient ectopic expression of miR-124 suppressed cell proliferation and survival, whereas genetic inhibition of this miRNA enhanced the fitness of these tumors. Mechanistically, the activities of miR-124 towards MYC and BCL2 intersect with both oncogenic and tumor-suppressive pathways. In respect to the former, we show that miR-124 directly targets nuclear factor-κB (NF-κB) p65, and using genetic approaches, we demonstrate that this interaction accounts for the miR-124-mediated suppression of MYC and BCL2. We also characterized miR-124 promoter region and identified a functional p53 binding site. In agreement with this finding, endogenous or ectopic expression of wild-type, but not mutant, p53 increased miR-124 levels and suppressed p65, MYC and BCL2. Our data unveil an miRNA-dependent regulatory circuitry that links p53 to the NF-κB pathway, which when disrupted in B-cell lymphoma may be associated with aberrant coexpression of MYC and BCL2 and poor prognosis.

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“…In HCC, miR-637 suppressed cell proliferation and enhanced cellular apoptosis through downregulation of STAT3 expression (41). miR-124 also inhibited HCC cell growth by directly targeting STAT3 (42). In pancreatic cancer, miR-130b decreased cell growth and invasion via inhibition of STAT3 (43).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125b targeted STAT3 to inhibit laryngeal squamous cell carcinoma cell growth and motility

et al. 2017

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Abstract.A majority of studies have indicated that microRNA-125b (miR-125b) is aberrantly expressed in various types of cancer. However, there are no studies on the expression and function of miR-125b in human laryngeal squamous cell carcinoma (LSCC). In the present study, miR-125b expression in LSCC sample tissues, corresponding adjacent non-neoplastic tissues, LSCC cell lines and a normal human keratinocyte cell line was measured using the reverse transcription-quantitative polymerase chain reaction. Following transfection with miR-125b mimics, the Cell Counting Kit-8, cell migration, cell invasion, western blotting and dual-luciferase reporter assays were performed on LSCC cell lines. According to the results, miR-125b was observed to be significantly downregulated in LSCC, and its expression was significantly associated with clinical stage and alcohol history. miR-125b was also observed to decrease cell growth, migra tion and invasion in LSCC cells by directly targeting signal transducer and activator of transcription 3. The results of the present study suggested that miR-125b may be a potential treatment target of LSCC in the future.

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MicroRNA-124 suppresses growth of human hepatocellular carcinoma by targeting STAT3

Cited by 68 publications

References 26 publications

MicroRNA-124 regulates glucocorticoid sensitivity by targeting phosphodiesterase 4B in diffuse large B cell lymphoma

MicroRNA-124 regulates glucocorticoid sensitivity by targeting phosphodiesterase 4B in diffuse large B cell lymphoma

MicroRNA-124 links p53 to the NF-κB pathway in B-cell lymphomas

MicroRNA-125b targeted STAT3 to inhibit laryngeal squamous cell carcinoma cell growth and motility

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