NOP14 suppresses breast cancer progression by inhibiting NRIP1/Wnt/β-catenin pathway

Lei, Jin; Peng, Rou Jun; Kuang, Bo Hua; Yuan, Zhong Yu; Tao, Qianshan; Liu, Wen Sheng; Guo, Yun; Han, Hui; Lian, Yi; Deng, Cheng; Zhang, Hao Jiong; Chen, Li Zhen; Feng, Qi Sheng; Xu, Miao; Lin, Feng; Bei, Jin Xin; Zeng, Yi Xin

doi:10.18632/oncotarget.4573

Cited by 29 publications

(33 citation statements)

References 33 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study demonstrated that NOP14 enhances the stability of mutp53, enabling mutp53 to participate in the progression of pancreatic cancer . NOP14 could suppress cancer metastasis by regulating the Wnt/β‐catenin signalling pathway in cancers . In our research, we found that NOP14 is involved in cell proliferation and migration and induces apoptosis in BCa cells.…”

Section: Discussionsupporting

confidence: 60%

“…35 NOP14 could suppress cancer metastasis by regulating the Wnt/β-catenin signalling pathway in cancers. 36,37 In our research, we found that NOP14 is involved in cell proliferation and migration and induces apoptosis in BCa cells. Furthermore, NOP14 silencing reduced the expression of cell cycle-related proteins and MMP9 and upregulated the expression of cleaved Caspase 3.…”

Section: Discussionmentioning

confidence: 56%

See 1 more Smart Citation

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Ying

Xie

et al. 2020

Cell Proliferation

View full text Add to dashboard Cite

Objectives Downregulation of miR‐502‐5p has emerged as a critical factor in tumour progression in several cancers. Herein, we elucidated the role of miR‐502‐5p in bladder cancer. Materials and methods RT‐qPCR was performed to examine the expression of miR‐502‐5p in bladder cancer. And DNA methylation analysis showed that epigenetic mechanisms may contribute to the downregulation of miR‐502‐5p. Then, wound‐healing assay, transwell assay, colony formation assay, CCK8 assay and flow cytometry analysis were applied to evaluate the function of miR‐502‐5p in bladder cancer cell lines. Western blot was conducted to measure the protein levels of related genes. Furthermore, dual‐luciferase reporter assay, in vivo tumorigenesis assay and immunohistochemical staining were also conducted as needed. Results MiR‐502‐5p is frequently downregulated in BCa. Meanwhile, hypermethylation of CpG islands contributes to the downregulation of miR‐502‐5p. Functionally, overexpression of miR‐502‐5p inhibited cell proliferation and migration in vitro and repressed tumour growth in vivo. CCND1, DNMT3B and NOP14 were identified as direct targets of miR‐502‐5p. Interestingly, DNMT3B and miR‐502‐5p established a positive feedback loop in the regulation of bladder cancer. In addition, rescue experiments further validated the direct molecular interaction between miR‐502‐5p and its targets. Conclusions Our study proposed and demonstrated that the miR‐502‐5p–mediated regulatory network is critical in bladder cancer; this network may be useful in the development of more effective therapies against bladder cancer.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 56%

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Ying

Xie

et al. 2020

Cell Proliferation

View full text Add to dashboard Cite

show abstract

“…Wnt/β-catenin signaling has been shown to play an important role in the development and promotion of into the nucleus of breast cancer cells. Additionally, in ER-positive breast cancers, NOP14 increase the level of ERα via NRIP1, implied that NOP14 can suppress breast cancer by inhibiting the Wnt/ β-catenin pathways possibly by up-regulating NRIP1 [25]. These findings provide new hope of developing targeted therapies against NOP14 and NRIP1 for breast cancer.…”

Section: Introductionmentioning

confidence: 82%

Advancement of Wnt signal pathway and the target of breast cancer

Qin

Zhao

et al. 2016

Open Life Sciences

View full text Add to dashboard Cite

Wnt/β-catenin signaling has been proved to play an important role in the development and promotion of cancer metastasis. The activation of Wnt signals can lead to duplicating, updating, metastasizing and relapsing. The Wnt signaling pathway is mainly divided into the Wnt/β-catenin pathway and the Wnt/calcium pathway. A better understanding of all the diverse functions of Wnt and their molecular mechanisms has evoked prevailing interest in identifying additional targets related to the Wnt /β-catenin pathways in breast cancer. A number of new target, related to Wnt /β-catenin pathways have been identified in recent years, including NOP14, BKCa channels, Emilin2, WISP, MicroRNAs, NRBP1, TRAF4, and Wntless. In this review, we will introduce the new targets related to the Wnt /β-catenin pathways in breast cancer.

show abstract

“…Eleven of the 12 sites were differentially edited including AZIN1 S367G , highlighting the importance of AZIN1 RNA editing in cancer development. The top 3 edited genes were NOP14 I779V (chr4:2,938,299), FLNB M2324V (chr3: 58,156,064), and IGFBP7 K95R (chr4: 57,110,068), all of which have been suggested to suppress breast cancer progression (26)(27)(28). Moreover, DNA mutations of NOP14 I779V and FLNB M2324V are reported in COSMIC (29), demonstrating the utility of TCEA to identify driver-like editing events in carcinogenesis.…”

Section: Edcancer Modulementioning

confidence: 94%

The Cancer Editome Atlas: A Resource for Exploratory Analysis of the Adenosine-to-Inosine RNA Editome in Cancer

Lin

Chen

2019

Cancer Research

View full text Add to dashboard Cite

Increasing evidence has suggested a role for adenosine-toinosine RNA editing in carcinogenesis. However, the clinical utility of RNA editing remains limited because functions of the vast majority of editing events remain largely unexplored. To help the cancer research community investigate functional consequences of individual editing events, we have developed a user-friendly bioinformatic resource, The Cancer Editome Atlas (TCEA; http://tcea.tmu.edu.tw). TCEA characterizes >192 million editing events at >4.6 million editing sites from approximately 11,000 samples across 33 cancer types in The Cancer Genome Atlas. Clinical information, miRNA expression , and alteration in miRNA targeting modulated through RNA editing are also integrated into TCEA. TCEA supports several modules to search, analyze, and visualize the cancer editome, providing a solid basis for investigating the oncogenic mechanisms of RNA editing and expediting the identification of therapeutic targets in cancer. Significance: This user-friendly bioinformatic resource reduces the barrier to analyzing the huge and complex cancer RNA editome that cancer researchers face and facilitates the identification of novel therapeutic targets in cancer.

show abstract

NOP14 suppresses breast cancer progression by inhibiting NRIP1/Wnt/β-catenin pathway

Cited by 29 publications

References 33 publications

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Advancement of Wnt signal pathway and the target of breast cancer

The Cancer Editome Atlas: A Resource for Exploratory Analysis of the Adenosine-to-Inosine RNA Editome in Cancer

Contact Info

Product

Resources

About