MYU, a Target lncRNA for Wnt/c-Myc Signaling, Mediates Induction of CDK6 to Promote Cell Cycle Progression

Kawasaki, Yuki; Komiya, M; Matsumura, Kosuke; Negishi, Lumi; Suda, Sakiko; Okuno, Masumi; Yokota, Naoko; Osada, Tomoya; Nagashima, Takeshi; Hiyoshi, Masaya; Okada‐Hatakeyama, Mariko; Kitayama, Joji; Shirahige, Katsuhiko; Akiyama, Tetsu

doi:10.1016/j.celrep.2016.08.015

Cited by 103 publications

(113 citation statements)

References 46 publications

(49 reference statements)

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“…ESRP1 binds to the SNAIL mRNA and promotes its SNAIL, while ESRP1 increases FGF7 expression and enhances the AKT signaling pathway downstream of the FGFR2 receptor in an autocrine fashion, resulting in increased SNAIL transcription and SNAIL protein stabilization . HNRNPK is often overexpressed in colorectal cancer cells, and, as mentioned in the Introduction, HNRNPK promotes their proliferation through stabilization of CDK6 mRNA, enhanced translation of mRNA encoding BTK , transcriptional control of CDKN2B , as well as through pre‐mRNA splicing of MRPL33 …”

Section: Discussionmentioning

confidence: 99%

HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells

et al. 2018

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Heterogeneous nuclear ribonucleoprotein L‐like (HNRNPLL), an RNA‐binding protein that regulates alternative splicing of pre‐mRNA, has been shown to regulate differentiation of lymphocytes, as well as metastasis of colorectal cancer cells. Here, we show that HNRNPLL promotes cell cycle progression and, hence, proliferation of colorectal cancer cells. Functional annotation analysis of those genes whose expression levels were changed threefold or more in RNA sequencing analysis between SW480 cells overexpressing HNRNPLL and those knocked down for HNRNPLL revealed enrichment of DNA replication‐related genes by HNRNPLL overexpression. Among 13 genes detected in the DNA replication pathway, PCNA,RFC3 and FEN1 showed reproducible upregulation by HNRNPLL overexpression both at mRNA and at protein levels in SW480 and HT29 cells. Importantly, knockdown of any of these genes alone suppressed the proliferation‐promoting effect induced by HNRNPLL overexpression. RNA‐immunoprecipitation assay presented a binding of FLAG‐tagged HNRNPLL to mRNA of these genes, and HNRNPLL overexpression significantly suppressed the downregulation of these genes during 12 h of actinomycin D treatment, suggesting a role of HNRNPLL in mRNA stability. Finally, analysis of a public RNA sequencing dataset of clinical samples suggested a link between overexpression of HNRNPLL and that of PCNA,RFC3 and FEN1. This link was further supported by immunohistochemistry of colorectal cancer clinical samples, whereas expression of CDKN1A, which is known to inhibit the cooperative function of PCNA, RFC3 and FEN1, was negatively associated with HNRNPLL expression. These results indicate that HNRNPLL stabilizes mRNA encoding regulators of DNA replication and promotes colorectal cancer cell proliferation.

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Section: Discussionmentioning

confidence: 99%

HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells

et al. 2018

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“…For cell synchronization, we used nocodazole (an inhibitor of tubulin assembly) as previously described . Forty‐eight hours after transfection, 5 μg/mL nocodazole was added to cells.…”

Section: Methodsmentioning

confidence: 99%

Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer

et al. 2019

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Alternative splicing, regulated by DEAD‐Box Helicase (DDX) families, plays an important role in cancer. However, the relationship between the DDX family and cancer has not been fully elucidated. In the present study, we identified a candidate oncogene DDX56 on Ch.7p by a bioinformatics approach using The Cancer Genome Atlas (TCGA) dataset of colorectal cancer (CRC). DDX56 expression was measured by RT‐qPCR and immunochemical staining in 108 CRC patients. Clinicopathological and survival analyses were carried out using three CRC datasets. Biological roles of DDX56 were explored by gene set enrichment analysis (GSEA), and cell proliferation in vitro and in vivo, cell cycle assays, and using DDX56‐knockdown or overexpressed CRC cells. RNA sequencing was carried out to elucidate the effect of DDX56 on mRNA splicing. We found that DDX56 expression was positively correlated with the amplification of DDX56 and was upregulated in CRC cells. High DDX56 expression was associated with lymphatic invasion and distant metastasis and was an independent poor prognostic factor. In vitro analysis, in vivo analysis and GSEA showed that DDX56 promoted proliferation ability through regulating the cell cycle. DDX56 knockdown reduced intron retention and tumor suppressor WEE1 expression, which functions as a G2‐M DNA damage checkpoint. We have identified DDX56 as a novel oncogene and prognostic biomarker of CRC that promotes alternative splicing of WEE1.

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“…As the development of biochips and sequencing technologies has advanced, it has become apparent that lncRNAs play critical roles in the pathogenesis of multiple diseases (Archer et al, 2015;Kawasaki et al, 2016). Although lncRNAs do not encode proteins, they do regulate a variety of genes that participate in cell signaling, controlling the expression of further genes, and cellular activities such as chromatin modification, epigenetic marking, and protein folding and activation (Froberg et al, 2013;Bassett et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells

2017

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ABSTRACT. The objective of this study was to investigate the effect of downregulating long non-coding RNAs (lncRNAs) on the reversal of cisplatin resistance in CP70 ovarian cancer cells, and to identify the underlying mechanism(s) of action. An lncRNA microarray was performed to screen for downregulated lncRNAs in cisplatin-resistant CP70 cells. Expression levels of these lncRNAs were then verified in SKOV3 and SKOV3/DDP cells. Quantitative polymerase chain reaction was conducted to identify the lncRNA most downregulated, which was then synthesized and transfected into CP70 cells. To assess the viability and migration ability of these transfected CP70 cells, methyl thiazolyl tetrazolium and Transwell assays were carried out. In addition, expression levels of apoptosis-related proteins were examined by western blotting. The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. Transfection of lncRNA ENST00000457645 into CP70 cells markedly inhibited viability and migration ability, and significantly increased expression of apoptotic proteins such as Bax and cleaved caspase-3. lncRNA ENST00000457645 negatively affects the viability and migration of cisplatin-resistant CP70 ovarian cancer cells. The mechanism responsible involves modification of apoptotic protein expression.

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MYU, a Target lncRNA for Wnt/c-Myc Signaling, Mediates Induction of CDK6 to Promote Cell Cycle Progression

Cited by 103 publications

References 46 publications

HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells

HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells

Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer

Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells

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