BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141

Liu, Yukun; Zhao, Ran; Wei, Yanmei; Li, Mengna; Wang, Heran; Niu, Weihong; Zhou, Yao; Qiu, Yuanzheng; Fan, Songqing; Zhan, Yihao; Wang, Xiong; Zhou, Yanhong; Li, Xiaoling; Li, Zheng; Li, Guiyuan; Zhou, Ming

doi:10.1186/s13046-018-0734-2

Cited by 29 publications

(34 citation statements)

References 44 publications

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“…Therefore, we first used dual-luciferase report assays and real-time PCR to detect the effect of YY1 on c-Myc-dependent miR-141 transcription and expression. As a result, ectopic expression of c-Myc led to the up-regulation of miR-141 promoter activity and expression, which is consistent with previous results (12), whereas YY1 overexpression decreases the effect of c-Myc on miR-141 promoter activity and expression in 5-8F and HNE2 cells ( Fig. 4, A and B).…”

Section: Yy1 Suppresses Cell Proliferation and Tumor Growth In Npc Yysupporting

confidence: 92%

“…Meanwhile, c-Myc was identified as a negative regulator of the bromodomain-containing protein 7 (BRD7) gene, which is a tumor suppressor in multiple types of cancers, as well as a cofactor of c-Myc (33)(34)(35). Therefore, BRD7 expression and c-Myc activation form a double-negative feedback loop that controls cell proliferation and tumor growth in NPC by target-ing the downstream gene miR-141 (12). In this study, we found that YY1 overexpression does not affect the mRNA and protein levels of c-Myc, but significantly reduces miR-141 expression, including pri-, pre-, and mature miR-141, as well as miR-141 promoter activity, suggesting that YY1 inhibits the activation of the c-Myc/miR-141 transcriptional axis.…”

Section: Yy1 Suppresses Cell Proliferation and Tumor Growth In Npcmentioning

confidence: 99%

“…The relative expression ratio of mature miR-141, pre-miR-141, and pri-miR-141 was calculated using the 2 Ϫ⌬⌬Ct method. The primers for miR-141, pre-miR141, U6, pri-miR141, c-Myc, and GAPDH were described previously (11,12). The relative amount of mRNA or gene to internal control was calculated using the equation 2 Ϫ⌬⌬Ct method.…”

Section: Rna Extraction and Quantitative Real-time Pcrmentioning

confidence: 99%

“…development and progression (10). Moreover, c-Myc is known to specifically bind the miR-141 promoter region and thus regulate the transcriptional activation of miR-141, whereas c-Myc knockdown has been shown to activate PTEN/AKT signaling and suppress cell proliferation and tumor growth via transcriptional down-regulation of miR-141 in NPC cells (11)(12)(13).…”

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confidence: 99%

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Zinc-finger protein YY1 suppresses tumor growth of human nasopharyngeal carcinoma by inactivating c-Myc–mediated microRNA-141 transcription

Liu

Wei

et al. 2019

Journal of Biological Chemistry

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Edited by Xiao-Fan WangYin Yang 1 (YY1) is a zinc-finger protein that plays critical roles in various biological processes by interacting with DNA and numerous protein partners. YY1 has been reported to play dual biological functions as either an oncogene or tumor suppressor in the development and progression of multiple cancers, but its role in human nasopharyngeal carcinoma (NPC) has not yet been revealed. In this study, we found that YY1 overexpression significantly inhibits cell proliferation and cell-cycle progression from G 1 to S and promotes apoptosis in NPC cells. Moreover, we identified YY1 as a component of the c-Myc complex and observed that ectopic expression of YY1 inhibits c-Myc transcriptional activity, as well as the promoter activity and expression of the c-Myc target gene microRNA-141 (miR-141). Furthermore, restoring miR-141 expression could at least partially reverse the inhibitory effect of YY1 on cell proliferation and tumor growth and on the expression of some critical c-Myc targets, such as PTEN/AKT pathway components both in vitro and in vivo.We also found that YY1 expression is reduced in NPC tissues, negatively correlates with miR-141 expression and clinical stages in NPC patients, and positively correlates with survival prognosis. Our results reveal a previously unappreciated mechanism in which the YY1/c-Myc/miR-141 axis plays a critical role in NPC progression and may provide some potential and valuable targets for the diagnosis and treatment of NPC.

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Section: Yy1 Suppresses Cell Proliferation and Tumor Growth In Npc Yysupporting

confidence: 92%

Section: Yy1 Suppresses Cell Proliferation and Tumor Growth In Npcmentioning

confidence: 99%

Section: Rna Extraction and Quantitative Real-time Pcrmentioning

confidence: 99%

mentioning

confidence: 99%

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Zinc-finger protein YY1 suppresses tumor growth of human nasopharyngeal carcinoma by inactivating c-Myc–mediated microRNA-141 transcription

Liu

Wei

et al. 2019

Journal of Biological Chemistry

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“…First strand cDNA synthesis with 2 μg of total RNAs was performed using a RevertAid first strand cDNA synthesis Kit according to the instructions (K1622, Thermo Scientific, USA). Detailed experimental procedures are referred to our published literature [22]. The gene expression was monitored using fluorescence quantitative PCR (CFX96, Bio-Rad, USA).…”

Section: Rna Extraction and Qrt-pcrmentioning

confidence: 99%

BRD7 suppresses invasion and metastasis in breast cancer by negatively regulating YB1-induced epithelial-mesenchymal transition

Niu

Luo

Zhou

et al. 2020

J Exp Clin Cancer Res

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Background: BRD7 is a tumor suppressor known to inhibit cell proliferation and cell cycle progression and initiate apoptosis in breast cancer. However, the function and underlying molecular events of BRD7 in tumor invasion and metastasis in breast cancer are not fully understood.Methods: BRD7 expression was assessed in two stable cell lines MDA231 and MCF7 with BRD7 overexpression and one stable cell line MDA231 with BRD7 interference using qRT-PCR and western blotting. CCK8 assay was used to examine the proliferation ability of MDA231 and MCF7 cells. Scratch wound healing assay was used to evaluate cell migration in MDA231 and MCF7 cells. Both Matrigel and three-dimensional invasion assays were performed to investigate the cell invasion ability after BRD7 overexpression or silencing or YB1 restoration in MDA231 and MCF7 cells. The potential interacting proteins of BRD7 were screened using co-immunoprecipitation combined with mass spectrometry and verified by co-immunoprecipitation in HEK293T cells. Additionally, we confirmed the specific binding region between BRD7 and YB1 in HEK293T cells by constructing a series of deletion mutants of BRD7 and YB1 respectively. Finally, xenograft and metastatic mouse models using MDA231 cells were established to confirm the effect of BRD7 on tumor growth and metastasis.Results: Here, the results of a series of assays in vitro indicated that BRD7 has the ability to inhibit the mobility, migration and invasion of breast cancer cells. In addition, YB1 was identified as a novel interacting protein of BRD7, and BRD7 was found to associate with the C-terminus of YB1 via its N-terminus. BRD7 decreases the expression of YB1 through negatively regulating YB1 phosphorylation at Ser102, thereby promoting its proteasomal degradation. Furthermore, gene set enrichment analysis revealed that epithelial-mesenchymal transition (EMT) is the common change occurring with altered expression of either BRD7 or YB1 and that BRD7 represses mesenchymal genes and activates epithelial genes. Moreover, restoring the expression of YB1 antagonized the inhibitory effect of BRD7 on tumorigenicity, EMT, invasiveness and metastasis through a series of in vitro and in vivo experiments. Additionally, BRD7 expression was negatively correlated with the level of YB1 in breast cancer patients. The combination of low BRD7 and high YB1 expression was significantly associated with poor prognosis, distant metastasis and advanced TNM stage.

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The emerging roles of the interaction between m6A modification and c‐Myc in driving tumorigenesis and development

Zheng

Wei

et al. 2022

Journal Cellular Physiology

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N6‐methyladenosine (m6A) is an extremely common and conservative posttranscriptional modification, that can specifically target and regulate the expression or stability of a series of tumor‐related genes, thus playing critical roles in the occurrence and development of tumors. c‐Myc is an important tumorigenic transcription factor that promotes tumorigenesis and development by mainly regulating the expression of downstream target genes. Increasing evidence shows that m6A modification, as well as abnormal expression and regulation of c‐Myc, is critical molecular mechanisms driving tumorigenesis and development. Although more evidence has been uncovered about the individual roles of m6A modification or c‐Myc in tumors, the interaction between m6A modification and c‐Myc in tumorigenesis and development has not been systematically summarized. Therefore, this review is focused on the mutual regulation between m6A modification and c‐Myc expression and stability as well as its roles in tumorigenesis and development. We also summarized the potential value of the interaction between m6A modification and m6A expression and stability in tumor diagnosis and treatment, which provides a specific reference for revealing the mechanism of tumor occurrence and development as well as clinical diagnosis and treatment.

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BRD7 expression and c-Myc activation forms a double-negative feedback loop that controls the cell proliferation and tumor growth of nasopharyngeal carcinoma by targeting oncogenic miR-141

Cited by 29 publications

References 44 publications

Zinc-finger protein YY1 suppresses tumor growth of human nasopharyngeal carcinoma by inactivating c-Myc–mediated microRNA-141 transcription

Zinc-finger protein YY1 suppresses tumor growth of human nasopharyngeal carcinoma by inactivating c-Myc–mediated microRNA-141 transcription

BRD7 suppresses invasion and metastasis in breast cancer by negatively regulating YB1-induced epithelial-mesenchymal transition

The emerging roles of the interaction between m6A modification and c‐Myc in driving tumorigenesis and development

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