A role of uridylation pathway for blockade of let‐7 micro<scp>RNA</scp> biogenesis by Lin28B

Suzuki, Hiroshi; Katsura, Akihiro; Miyazono, Kohei

doi:10.1111/cas.12721

Cited by 25 publications

(28 citation statements)

References 48 publications

(87 reference statements)

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“…Lin28A/B enhances the growth of breast and colon tumors via inhibition of let-7 miRNA biogenesis. 30 These reports strongly support our current data: we indicated that NF90 induces CRC angiogenesis, growth, and metastasis through suppression of pri-miR-590 processing by binding of NF90 to pri-miR-590, thus decreasing the levels of mature miR-590-5p. Interestingly, it has been reported that NF90 or the NF90-NF45 complex is involved in mRNA stabilization and transcription.…”

Section: Discussionsupporting

confidence: 91%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.

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Section: Discussionsupporting

confidence: 91%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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“…To our knowledge, this study may provide the first evidence that AC105461.1 is likely to negatively correlate with tumor progression. In addition, further studies declare that DIS3L2 is strongly linked with Lin28/let-7 pathway which is relevant to various cancers 17,26,27. The need for further analyses of the exact regulation mechanism and the relationship between AC105461.1 and Lin28/let-7 pathway are unmet.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of a DIS3L2 promoter upstream long noncoding RNA (AC105461.1) enhances colorectal cancer stem cell properties in vitro by down-regulating DIS3L2

Liu¹,

Yu²,

Ma³

et al. 2017

OTT

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A large number of studies have identified plentiful long noncoding RNAs (lncRNAs) associated with the development of multiple cancers. Some lncRNAs have also been found to be strongly linked with stem cell properties such as pluripotency and differentiation. However, only in a few cases have cancer stem cell (CSC)-related lncRNAs been studied. Commonly, the expression and function of lncRNAs are associated with adjacent protein coding transcripts. In the present study, we found an lncRNA (AC105461.1), a promoter upstream transcript of DIS3 mitotic control homolog (Saccharomyces cerevisiae)-like 2 (DIS3L2), may be closely connected with “stem cell-like” properties. We firstly investigated whether the expression of AC105461.1 was down-regulated in colorectal cancer (CRC) tissue samples. Subsequently, we explored the expression pattern of the lncRNA/mRNA gene pair between AC105461.1 and DIS3L2 in 47 CRC specimens by real-time polymerase chain reaction. The results showed that the expression of AC105461.1 was positively correlated with that of DIS3L2. Through CRC cell lines screening experiment, we found that AC105461.1 expression was highest in SW480 and lowest in SW620 cells. Moreover, the results obtained by overexpression experiment indicated that AC105461.1 expression was markedly elevated and DIS3L2 expression level was also apparently upregulated by plasmid cDNA-AC105461.1. In contrast, we further found that AC105461.1 expression level in AC105461.1 siRNA group was significantly knocked down in SW480 cells. Meanwhile, DIS3L2 expression was also markedly decreased. Importantly, we noticed that AC105461.1 overexpression impaired CSC properties, while its knockdown enhanced CSC properties, including self-renewal, migration, and invasion abilities. To further identify the influence of AC105461.1 expression on CSCs properties in CRC, CD133 and CD44, as current universal markers for characterizing CRC stem cells, were selected to perform flow cytometry analysis. As a result, we found that AC105461.1 overexpression reduced the percentage of CD133+CD44+, whereas its knockdown increased the percentage of CD133+CD44+. Taken together, our findings indicated that AC105461.1 may be a regulator of DIS3L2 and a mediator of CRC stem cells, and we speculate that AC105461.1 could be regarded as a promising biomarker and therapeutic target for CRC.

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“…let‐7 is expressed in differentiated cells where it negatively regulates several known oncogenes, but is repressed in embryonic stem cells and in several cancers in mammals . A prominent factor regulating let‐7 accumulation is the RNA‐binding protein Lin28 . The genome of vertebrates encodes two paralogous Lin28 proteins.…”

Section: Dual Role Of Uridylation In Let‐7 Mirna Biogenesismentioning

confidence: 99%

“…69,70 A prominent factor regulating let-7 accumulation is the RNA-binding protein Lin28. [30][31][32]41,[70][71][72][73][74][75] The genome of vertebrates encodes two paralogous Lin28 proteins. Both Lin28A and Lin28B downregulate let-7 production by distinct mechanisms including the sequestration of precursors away from nuclear processing factors and uridylation -mediated degradation of cytosolic precursors (2), the precursors undergo a first uridylation step by RET1 (3), leading to the degradation of the precursors by DSS1 (4).…”

Section: Dual Role Of Uridylation In Let-7 Mirna Biogenesismentioning

confidence: 99%

“…73 Lin28B was also reported to promote uridylation and Dis3L2-mediated degradation of pre-let-7 miRNAs in certain cancer cells. 72 Altogether, studies of let-7 biogenesis revealed a fascinating regulatory role of RNA snRNAs are transcribed by polymerase III (Pol III) which terminates transcription by a stretch of four encoded uridines (1) that are immediately bound by the La protein (2). U6 snRNAs are then uridylated by U6 TUTase (TUT1) (3) which favors nibbling by the exoribonuclease Usb1 (4).…”

Section: Boxmentioning

confidence: 99%

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RNA uridylation: a key posttranscriptional modification shaping the coding and noncoding transcriptome

et al. 2017

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RNA uridylation is a potent and widespread posttranscriptional regulator of gene expression. RNA uridylation has been detected in a range of eukaryotes including trypanosomes, animals, plants, and fungi, but with the noticeable exception of budding yeast. Virtually all classes of eukaryotic RNAs can be uridylated and uridylation can also tag viral RNAs. The untemplated addition of a few uridines at the 3 0 end of a transcript can have a decisive impact on RNA's fate. In rare instances, uridylation is an intrinsic step in the maturation of noncoding RNAs like for the U6 spliceosomal RNA or mitochondrial guide RNAs in trypanosomes. Uridylation can also switch specific miRNA precursors from a degradative to a processing mode. This switch depends on the number of uridines added which is regulated by the cellular context. Yet, the typical consequence of uridylation on mature noncoding RNAs or their precursors is to accelerate decay. Importantly, mRNAs are also tagged by uridylation. In fact, the advent of novel high throughput sequencing protocols has recently revealed the pervasiveness of mRNA uridylation, from plants to humans. As for noncoding RNAs, the main function to date for mRNA uridylation is to promote degradation. Yet, additional roles begin to be ascribed to U-tailing such as the control of mRNA deadenylation, translation control and possibly storage. All these new findings illustrate that we are just beginning to appreciate the diversity of roles played by RNA uridylation and its full temporal and spatial implication in regulating gene expression.

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A role of uridylation pathway for blockade of let‐7 microRNA biogenesis by Lin28B

Cited by 25 publications

References 48 publications

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

Knockdown of a DIS3L2 promoter upstream long noncoding RNA (AC105461.1) enhances colorectal cancer stem cell properties in vitro by down-regulating DIS3L2

RNA uridylation: a key posttranscriptional modification shaping the coding and noncoding transcriptome

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