The new world of RNAs

Dogini, D.B.; Pascoal, Vinícius D'Ávila Bitencourt; Avansini, Simoni Helena; Vieira, André Schwambach; Pereira, Tiago Campos; Lopes-Cendes, Íscia

doi:10.1590/s1415-47572014000200014

Cited by 93 publications

(56 citation statements)

References 124 publications

(140 reference statements)

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“…In the present study, siRNA technology was used, and double-stranded siRNA targeting β-catenin was synthesized (15)(16)(17). The experimental results indicated that specific siRNA targeting β-catenin could inhibit the expression of the β-catenin gene.…”

Section: Discussionmentioning

confidence: 93%

Knockdown of β-catenin by siRNA influences proliferation, apoptosis and invasion of the colon cancer cell line SW480

Zhou

et al. 2016

Oncology Letters

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Abstract. The aim of the present study was to explore the effect of knocking down the expression of β-catenin by small interference (si)RNA on the activity of the Wnt/β-catenin signaling pathway, and the proliferation, apoptosis and invasion abilities of the human colon cancer cell line SW480. For that purpose, double-stranded siRNA targeting β-catenin (β-catenin-siRNA) was synthesized and transfected into SW480 cells. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to detect the messenger (m)RNA and protein levels of β-catenin in SW480 cells. To detect cell proliferation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed, while cell apoptosis and caspase-3 activity were detected by flow cytometry and caspase-3 activity assay, respectively. Matrigel invasion assay was performed to detect the influence of siRNA-mediated gene silencing on the invasion and metastasis of SW480 cells in vitro. The results of RT-PCR and western blot analysis demonstrated that, compared with the blank control, negative control and liposome groups, β-catenin-siRNA transfected SW480 cells had significantly decreased mRNA and protein levels of β-catenin. In addition, following β-catenin-siRNA transfection, the proliferation of SW480 cells was significantly lower than that of the blank control, negative control and liposome groups, while the apoptosis rate increased in β-catenin-siRNA transfected cells, compared with the aforementioned groups. Invasion assay showed that, following β-catenin-siRNA transfection, the number of SW480 cells infiltrating through the Matrigel membrane was significantly lower than that of the blank control, negative control and liposome groups. Following β-catenin-siRNA transfection, the caspase-3 activity in SW480 cells was lower than that in the blank control, negative control and liposome groups. These results indicate that siRNA-mediated silencing of β-catenin could inhibit the proliferation and invasion of SW480 cells and induce apoptosis, thus providing novel potential strategies for the clinical treatment of colon cancer, and may serve as a novel target for cancer therapy.

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Section: Discussionmentioning

confidence: 93%

Knockdown of β-catenin by siRNA influences proliferation, apoptosis and invasion of the colon cancer cell line SW480

Zhou

et al. 2016

Oncology Letters

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“…miR-195 has also been suggested to be useful as a potential diagnostic and therapeutic target for breast cancer (8,9), and has been shown to inhibit bladder cancer cell proliferation by directly targeting CDK4 and GLUT3 (10,11). As one miRNA has multiple targets, and one mRNA can be targeted by numerous miRNAs (12), the underlying molecular mechanisms of miR-195 in bladder cancer, and the existence of other targets of miR-195, remain unclear.…”

Section: Introductionmentioning

confidence: 99%

microRNA-195 inhibits cell proliferation in bladder cancer via inhibition of cell division control protein 42 homolog/signal transducer and activator of transcription-3 signaling

Zhao¹,

Lin²,

Chen³

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. microRNA (miR)-195 acts as a suppressor in multiple types of malignant tumors, including bladder cancer; however, the detailed function of miR-195 in bladder cancer remains largely unknown. The aim of the present study was to investigate the role of miR-195 in the regulation of bladder cancer cell proliferation and to determine whether cell division control protein 42 homolog (Cdc42)/signal transducer and activator of transcription-3 (STAT3) signaling acts as a downstream effector of miR-195 in bladder cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to determine the expression levels of miR-195 in bladder cancer tissues and normal adjacent tissue. The results revealed that the expression of miR-195 was significantly downregulated in bladder cancer tissues compared with that in the normal adjacent tissues. A luciferase reporter assay was then conducted, which identified Cdc42 as a direct target of miR-195, and the expression of Cdc42 was significantly upregulated in bladder cancer tissues, as determined by western blotting. Furthermore, miR-195 negatively regulated the protein expression of Cdc42 in bladder cancer cells. An MTT assay was also conducted to determine the rate of cell proliferation. Upregulation of miR-195 or the inhibition of Cdc42 could inhibit bladder cancer cell proliferation, possibly through activation of STAT3 signaling. In addition, restoration of Cdc42 could reverse the inhibitory effect of miR-195 upregulation on bladder cancer cell proliferation. In conclusion, the results of the present study suggest that miR-195 plays an inhibitory role in the regulation of bladder cancer cell proliferation by directly targeting Cdc42/STAT3 signaling.

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“…MicroRNAs (miRNAs) belong to a class of small endogenous non-coding RNAs with $22nt that repress mRNA of protein-coding translation by base pairing of the target genes [4]. It has been shown that miRNAs regulate the expression of at least one-third of all human genes [5], and bioinformatics analyses estimate that more than 60% of human protein-coding genes maintain pairing to miRNAs with regulatory roles in cell proliferation, differentiation, apoptosis, pathogenesis of many human diseases and tumorigenesis [6][7][8][9][10][11]. The loss or dysregulation of certain individual miRNAs can have serious physiological consequences [12][13][14].…”

Section: T Cell Receptor (Tcr)abmentioning

confidence: 99%

Differential regulation of miR-146a/FAS and miR-21/FASLG axes in autoimmune lymphoproliferative syndrome due to FAS mutation (ALPS-FAS)

Marega

Teocchi

Vilela

2016

Clinical and Experimental Immunology

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1These authors contributed equally to the study. SummaryMost cases of autoimmune lymphoproliferative syndrome (ALPS) have an inherited genetic defect involving apoptosis-related genes of the FAS pathway. MicroRNAs (miRNAs) are a class of small non-coding regulatory RNAs playing a role in the control of gene expression. This is the first report on miRNAs in ALPS patients. We studied a mother and son carrying the same FAS cell surface death receptor (FAS) mutation, but with only the son manifesting the signs and symptoms of ALPS-FAS. The aim was to analyse, by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), the peripheral blood mononuclear cells (PBMC) relative expression of miR-146a and miR-21, including their passenger strands and respective targets (FAS and FASLG). In comparison with healthy matched control individuals, miR-21-3p was over-expressed significantly (P 5 0Á0313) in the son, with no significant change in the expression of miR-146a, miR-146a-3p and miR-21. In contrast, the mother had a slight under-expression of the miR-146a pair and miR-21-3p (P 5 0Á0625). Regarding the miRNA targets, FAS was up-regulated markedly for the mother (P 5 0Á0078), but down-regulated for the son (P 5 0Á0625), while FASLG did not have any significant alteration. Taken together, our finding clearly suggests a role of the miR-146a/FAS axis in ALPS-FAS variable expressivity in which FAS haploinsufficiency seems to be compensated only in the mother who had the miR-146a pair down-regulated. As only the son had the major clinical manifestations of ALPS-FAS, miR-21-3p should be investigated as playing a critical role in ALPS physiopathology, including the development of lymphoma.

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The new world of RNAs

Cited by 93 publications

References 124 publications

Knockdown of β-catenin by siRNA influences proliferation, apoptosis and invasion of the colon cancer cell line SW480

Knockdown of β-catenin by siRNA influences proliferation, apoptosis and invasion of the colon cancer cell line SW480

microRNA-195 inhibits cell proliferation in bladder cancer via inhibition of cell division control protein 42 homolog/signal transducer and activator of transcription-3 signaling

Differential regulation of miR-146a/FAS and miR-21/FASLG axes in autoimmune lymphoproliferative syndrome due to FAS mutation (ALPS-FAS)

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