Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Pei, Hailong; Hu, Wentao; Guo, Ziyang; Chen, Huaiyuan; Ma, Ji; Mao, Weidong; Li, Bingyan; Wang, Aiqing; Wan, Jian; Zhang, Jian; Nie, Jing; Zhou, Guangming; Hei, Tom K.

doi:10.1158/0008-5472.can-18-0988

Cited by 29 publications

(33 citation statements)

References 43 publications

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“…LNC CRYBG3 is present in the human lung, brain, liver, and kidney, and is transcribed from the crystallin beta-gamma domain containing 3 (CRYBG3) gene on chromosome 3 (http://www.noncode.org/). In a previous study, we reported that LNC CRYBG3 directly binds to G-actin and suppresses G-actin assembly 19. Consistently, in the present study, unsupervised hierarchical clustering analysis of the expression of 1501 proteins showed that actin was the most downregulated.…”

Section: Discussionsupporting

confidence: 91%

LNC CRYBG3 inhibits tumor growth by inducing M phase arrest

et al. 2019

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Long noncoding RNAs (lncRNAs) are usually associated with tumor development and progression and some of them are dysregulated in various human cancers. The mechanisms underlying their dysregulation are worth further study. Here, we demonstrate that the expression level of LNC CRYBG3 is correlated with 1501 aberrantly expressed proteins in A549 cells (non-small cell lung cancer (NSCLC) cells). LNC CRYBG3 overexpression results in M phase arrest and promoted cell death, whereas LNC CRYBG3 knockdown did not elicit the opposite effects. The overexpression of LNC CRYBG3 inhibits cell proliferation both in vitro and in vivo. Moreover, it upregulates the expression of cyclin B1 and the phosphorylation of H3, whereas it inhibited the expression of cyclin-dependent kinase 6 and cyclin D1. Taken together, these findings suggest that LNC CRYBG3 regulates the cell cycle process of A549 cells, suggesting its potential application for the treatment of this disease.

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Section: Discussionsupporting

confidence: 91%

LNC CRYBG3 inhibits tumor growth by inducing M phase arrest

et al. 2019

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“…In this regard, lncRNA CRYBG3 has been shown to interact with G-actin to inhibit its polymerization such that this interaction between CRYBG3 and G-actin blocks nuclear localization of MAL. A consequence is that SRF is kept away from the promoter region of several immediate early genes such as JUNB and Arp3 82 . Finally, direct interaction of lncRNAs with target proteins can also impact their nuclear trafficking.…”

Section: Post-transcriptional Regulation Of Gene Expressionmentioning

confidence: 99%

Emerging roles of lncRNAs in the post-transcriptional regulation in cancer

Luo²,

2019

Genes & Diseases

197

127

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Accumulating evidence indicates that long non-coding RNAs (lncRNAs) can play a pivotal role in regulation of diverse cellular processes. In particular, lncRNAs can serve as master gene regulators at transcriptional and posttranscriptional levels, leading to tumorigenesis. In this review, we discuss latest developments in lncRNA-meditated gene expression at the post-transcriptional level, including gene splicing, mRNA stability, protein stability and nuclear trafficking.

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“…Regulating of cell cycle progression is another paramount mechanism to modulate tumor cell biological behavior (88). Various studies have reported divergent effects of BRACHYURY on cell proliferation.…”

Section: The Effect Of Brachyury On Tumor Cell Proliferation and Cellmentioning

confidence: 99%

The Roles of Embryonic Transcription Factor BRACHYURY in Tumorigenesis and Progression

Chen

Zhang

et al. 2020

Front. Oncol.

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Transcription factor brachyury, with a DNA-binding T-domain, regulates posterior mesoderm formation and notochord development through binding with highly conserved palindromic consensus sequence in a variety of organisms. The absence of brachyury expression in majority of adult normal tissues and exclusive tumor-specific expression provides the potential to be developed into a novel and promising diagnostic and therapeutic target in cancer. As a sensitive and specific marker in the diagnosis of chordoma, brachyury protein has been verified to involve in the process of carcinogenesis and progression of chordoma and several epithelial carcinomas in various studies, but the mechanism by which brachyury promotes tumor cells migrate, invade and metastasis still remains less clear. To this end, we attempt to summarize the literature on the upstream regulatory pathway of brachyury transcription and downstream controlling network by brachyury activation, all of which involve in both the embryonic development and tumor progression. We present the respective correlation of brachyury expression with tumor progression, distant metastasis, survival rate and prognosis in several types of tumor samples (including chordoma, lung cancer, breast carcinoma, and prostate cancer), and various brachyury gain-of-function and loss-of-function experiments are summarized to explore its specific role in respective tumor cell line in vitro. In addition, we also discuss another two programs relating to brachyury function: epithelial-to-mesenchymal transition (EMT) and cell cycle control, both of which implicate in the regulation of brachyury on biological behavior of tumor cells. This review will provide an overview of the function of master transcriptional factor brachyury, compare the similarities and differences of its role between embryonic development and carcinogenesis, and list the evidence on which brachyury-target therapies have the potential to help control advanced cancer populations.

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Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Cited by 29 publications

References 43 publications

LNC CRYBG3 inhibits tumor growth by inducing M phase arrest

LNC CRYBG3 inhibits tumor growth by inducing M phase arrest

Emerging roles of lncRNAs in the post-transcriptional regulation in cancer

The Roles of Embryonic Transcription Factor BRACHYURY in Tumorigenesis and Progression

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