scholarly journals A Distinct Expression Pattern of the Long 3′-Untranslated Region Dicer mRNA and Its Implications for Posttranscriptional Regulation in Colorectal Cancer

2012 ◽  
Vol 3 (7) ◽  
pp. e17 ◽  
Author(s):  
Yasushi Hamaya ◽  
Shigeru Kuriyama ◽  
Tetsunari Takai ◽  
Ken-ichi Yoshida ◽  
Takanori Yamada ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Expression Pattern ◽  
Posttranscriptional Regulation ◽  
Untranslated Region

scholarly journals The Molecular Basis and Therapeutic Potential of Let-7 MicroRNAs against Colorectal Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Rei Mizuno ◽  
Kenji Kawada ◽  
Yoshiharu Sakai
Keyword(s):  
Colorectal Cancer ◽  
Molecular Basis ◽  
Posttranscriptional Regulation ◽  
Therapeutic Agent ◽  
Therapeutic Potential ◽  
Noncoding Rnas ◽  
Intestinal Tumorigenesis ◽  
C Elegans ◽  
Microrna Family ◽  
Underlying Mechanisms

Although a number of studies have revealed the underlying mechanisms which regulate the development of colorectal cancer (CRC), we have not completely overcome this disease yet. Accumulating evidence has shown that the posttranscriptional regulation by the noncoding RNAs such as microRNAs plays an important role in the development or progression of CRC. Among a number of microRNAs, the let-7 microRNA family that was first discovered in C. elegans and conserved from worms to humans has been linked with the development of many types of cancers including CRC. The expression level of let-7 microRNAs is temporally low during the normal developmental processes, while elevated in the differentiated tissues. The let-7 microRNAs regulate the cell proliferation, cell cycle, apoptosis, metabolism, and stemness. In CRC, expressions of let-7 microRNAs have been reported to be reduced, and so let-7 microRNAs are considered to be a tumor suppressor. In this review, we discuss the mechanisms regulating the let-7 microRNA expression and the downstream targets of let-7 in the context of intestinal tumorigenesis. The application of let-7 mimics is also highlighted as a novel therapeutic agent.

scholarly journals Nkx2.5 Functions as a Conditional Tumor Suppressor Gene in Colorectal Cancer Cells via Acting as a Transcriptional Coactivator in p53-Mediated p21 Expression

2021 ◽  
Vol 11 ◽  
Author(s):  
Huili Li ◽  
Jiliang Wang ◽  
Kun Huang ◽  
Tao Zhang ◽  
Lu Gao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Expression Pattern ◽  
Cell Lines ◽  
Suppressor Gene ◽  
Transcriptional Coactivator ◽  
Wild Type ◽  
Mutational Status ◽  
Sw480 Cells

NK2 homeobox 5 (Nkx2.5), a homeobox-containing transcription factor, is associated with a spectrum of congenital heart diseases. Recently, Nkx2.5 was also found to be differentially expressed in several kinds of tumors. In colorectal cancer (CRC) tissue and cells, hypermethylation of Nkx2.5 was observed. However, the roles of Nkx2.5 in CRC cells have not been fully elucidated. In the present study, we assessed the relationship between Nkx2.5 and CRC by analyzing the expression pattern of Nkx2.5 in CRC samples and the adjacent normal colonic mucosa (NCM) samples, as well as in CRC cell lines. We found higher expression of Nkx2.5 in CRC compared with NCM samples. CRC cell lines with poorer differentiation also had higher expression of Nkx2.5. Although this expression pattern makes Nkx2.5 seem like an oncogene, in vitro and in vivo tumor suppressive effects of Nkx2.5 were detected in HCT116 cells by establishing Nkx2.5-overexpressed CRC cells. However, Nkx2.5 overexpression was incapacitated in SW480 cells. To further assess the mechanism, different expression levels and mutational status of p53 were observed in HCT116 and SW480 cells. The expression of p21WAF1/CIP1, a downstream antitumor effector of p53, in CRC cells depends on both expression level and mutational status of p53. Overexpressed Nkx2.5 could elevate the expression of p21WAF1/CIP1 only in CRC cells with wild-type p53 (HCT116), rather than in CRC cells with mutated p53 (SW480). Mechanistically, Nkx2.5 could interact with p53 and increase the transcription of p21WAF1/CIP1 without affecting the expression of p53. In conclusion, our findings demonstrate that Nkx2.5 could act as a conditional tumor suppressor gene in CRC cells with respect to the mutational status of p53. The tumor suppressive effect of Nkx2.5 could be mediated by its role as a transcriptional coactivator in wild-type p53-mediated p21WAF1/CIP1 expression.

scholarly journals Expression of thyroid hormone receptors A and B in developing rat tissues; evidence for extensive posttranscriptional regulation

2007 ◽  
Vol 38 (5) ◽  
pp. 523-535 ◽  
Author(s):  
Richard Keijzer ◽  
Piet-Jan E Blommaart ◽  
Wil T Labruyère ◽  
Jacqueline L M Vermeulen ◽  
Behrouz Zandieh Doulabi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Expression Pattern ◽  
Posttranscriptional Regulation ◽  
Time Course ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Tissue Expression ◽  
Translational Efficiency ◽  
Rat Tissues ◽  
High Turnover

The perinatal changes in the pattern of expression of the thyroid hormone receptor (TR) isoforms TRα 1 TRα 2, TRβ 1, and TRβ 2 were investigated using in situ hybridization and immunohistochemistry, and RT-PCR and western blotting as visualization and quantification techniques respectively. In liver, lung, and kidney, TRα mRNA was expressed in the stromal and TRβ mRNA in the parenchymal component of the tissues. When compared with liver, TRα mRNA concentrations were tenfold higher in lung, kidney, and intestine, and 100-fold higher in brain, with TRα 2 mRNA concentrations exceeding those of TRα 1 5-to 10-fold. Tissue TRβ 1 mRNA concentrations were similar in liver, lung, and brain, and 3- to 5-fold higher in kidney and intestine. None of the TRβ 2 mRNA could be detected outside the pituitary. Tissue TRα 2 and TRβ 1 protein levels reached adult levels at 5 days before birth, whereas TRα 1 protein peaked after birth. Because of the distinct time-course of thyroid hormone-binding receptors TRα 1 and TRβ 1, we speculate that an initiating, TRβ 1-mediated signaling from the parenchyma is followed by a TRα 1-mediated response in the stroma. When compared with organs with a complementary parenchymal–stromal expression pattern, organs with extensive cellular co-expression of TRα and TRβ (brain and intestinal epithelium) were characterized by a very low TRα protein: mRNA ratio, implying a low translational efficiency of TR mRNA or a high turnover of TR protein. The data indicate that the TR-dependent regulatory cascades are controlled differently in organs with a complementary tissue expression pattern and in those with cellular co-expression of the TRα and TRβ genes.

Circular RNAs as biomarkers in liquid biopsy in colorectal cancer.

2020 ◽  
Vol 38 (4_suppl) ◽  
pp. 230-230
Author(s):  
Manuel Valladares-Ayerbes ◽  
Carmen Garrigos ◽  
Miquel Taron ◽  
Angélica Figueroa ◽  
Enrique Aranda
Keyword(s):  
Colorectal Cancer ◽  
Bone Marrow ◽  
Expression Pattern ◽  
Liquid Biopsy ◽  
Expression Patterns ◽  
Target Prediction ◽  
Differentially Expressed ◽  
Circular Rnas ◽  
Blood Leukocytes ◽  
Specific Expression

230 Background: Circular RNAs (circRNAs) are emerging as essential regulators of cancer- related biological hallmarks, as cell proliferation, apoptosis, differentiation, immune regulation and angiogenesis. CircRNAs are abundant, conserved, and have a tissue‐specific expression pattern. These characteristics make them candidate to serve as biomarkers in liquid biopsy (LB) in cancer. The aim of this study is to analyse differential expression of circRNAs in the colorectal cancer (CRC) scenario. Methods: To comprehensively understand the expression patterns of circRNAs we characterized 13,617 circRNAs using a microarray [Arraystar v2 (8x15K)] in 10 human samples, five CRC cell lines, one colorectal human tumour, one normal colon healthy control, vs. Peripheral Human Blood Leukocytes (2 pools) and Human Bone Marrow. Differentially expressed circRNAs were identified using fold change (FC) cut-off or through Volcano Plot filtering respectively. CircRNAs having FC ▪2 and P-values ▪ 0.05 were selected. CircRNA/microRNA interaction was predicted with target prediction software. Results: Hierarchical clustering showed distinguishable circRNA expression profiling among 10 samples. These data indicated that circRNAs have a different expression pattern in colorectal tissues compared with that in blood and bone marrow tissues. The microarray data showed 2329 circRNAs differentially expressed (FC > 2.0, P < 0.05). Among them, 964 circRNAs were upregulated and 1365 were downregulated in colon tissues compared with blood and bone marrow. Using a stringent criterion (FC > 10, P≤ 0.01 and false discovery rate [FDR] < 0.05) we have identified 30 circRNA upregulated in colorectal cancer versus non tumour samples. CircRNA/microRNA interaction prediction analysis showed that most upregulated circRNAs contain miRNA Binding Sites (MREs) for cancer-related miRNA, including among others, miR-17, miR-103, miR-let-7g. Conclusions: Microarray analysis was used to comprehensively identify dysregulated circRNAs in CRC. We identify novel circRNAs could be valuable as blood-based CRC biomarkers.

scholarly journals Colorectal Cancer: From the Genetic Model to Posttranscriptional Regulation by Noncoding RNAs

2017 ◽  
Vol 2017 ◽  
pp. 1-38 ◽  
Author(s):  
María Antonia Lizarbe ◽  
Jorge Calle-Espinosa ◽  
Eva Fernández-Lizarbe ◽  
Sara Fernández-Lizarbe ◽  
Miguel Ángel Robles ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Posttranscriptional Regulation ◽  
Genetic Model ◽  
Treatment Options ◽  
Noncoding Rnas ◽  
Developed Countries ◽  
Colorectal Carcinogenesis ◽  
Special Focus ◽  
Epigenetic Alterations ◽  
And Function

Colorectal cancer is the third most common form of cancer in developed countries and, despite the improvements achieved in its treatment options, remains as one of the main causes of cancer-related death. In this review, we first focus on colorectal carcinogenesis and on the genetic and epigenetic alterations involved. In addition, noncoding RNAs have been shown to be important regulators of gene expression. We present a general overview of what is known about these molecules and their role and dysregulation in cancer, with a special focus on the biogenesis, characteristics, and function of microRNAs. These molecules are important regulators of carcinogenesis, progression, invasion, angiogenesis, and metastases in cancer, including colorectal cancer. For this reason, miRNAs can be used as potential biomarkers for diagnosis, prognosis, and efficacy of chemotherapeutic treatments, or even as therapeutic agents, or as targets by themselves. Thus, this review highlights the importance of miRNAs in the development, progression, diagnosis, and therapy of colorectal cancer and summarizes current therapeutic approaches for the treatment of colorectal cancer.

scholarly journals The Inhibitory Activity of the AU-Rich RNA Element in the Human Papillomavirus Type 1 Late 3′ Untranslated Region Correlates with Its Affinity for the elav-Like HuR Protein

1999 ◽  
Vol 73 (2) ◽  
pp. 1080-1091 ◽  
Author(s):  
Marcus Sokolowski ◽  
Henry Furneaux ◽  
Stefan Schwartz
Keyword(s):  
Human Papillomavirus ◽  
Posttranscriptional Regulation ◽  
Untranslated Region ◽  
Late Gene ◽  
Wild Type ◽  
Late Gene Expression ◽  
Transfected Cells ◽  
Type Sequence

ABSTRACT A 57-nucleotide adenosine- and uridine-rich RNA instability element in the human papillomavirus type 1 late 3′ untranslated region termedh1ARE has previously been shown to interact specifically with three nuclear proteins that failed to bind to an inactive mutant RNA. Two of those were identified as the heterogeneous ribonucleoproteins C1 and C2, whereas the third, a 38-kDa, poly(U) binding protein (p38), remained unidentified. Here we show that partially purified p38 reacts with a monoclonal antibody raised against the recently identified elav-like HuR protein, indicating that p38 is the HuR protein. Indeed, recombinant glutathioneS-transferase (GST)-HuR protein binds specifically to sites within the h1ARE. Determination of the apparentKd value of GST-HuR for the h1ARE and the inactive mutant thereof revealed that GST-HuR bound with a more than 50-fold-higher affinity to the wild-type sequence. Therefore, the binding affinity of GST-HuR for the wild-type and mutanth1AREs correlates with their inhibitory activities in transfected cells, strongly suggesting that the HuR protein is involved in the posttranscriptional regulation of human papillomavirus type 1 late-gene expression.

scholarly journals Correction: Posttranscriptional regulation of Galectin-3 by miR-128 contributes to colorectal cancer progression

Oncotarget ◽  
2018 ◽  
Vol 9 (15) ◽  
pp. 12535-12535
Author(s):  
Weiqun Lu ◽  
Jia Wang ◽  
Guohua Yang ◽  
Nanrong Yu ◽  
Zhiliang Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Posttranscriptional Regulation ◽  
Galectin 3 ◽  
Colorectal Cancer Progression
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