scholarly journals Exploration of small RNA-seq data for small non-coding RNAs in Human Colorectal Cancer

2017 ◽  
Vol 5 ◽  
pp. 16-31 ◽  
Author(s):  
Srinivas V Koduru ◽  
Amit K Tiwari ◽  
Sprague W Hazard ◽  
Milind Mahajan ◽  
Dino J Ravnic
Keyword(s):  
Colorectal Cancer ◽  
Small Rna ◽  
Rna Seq ◽  
Human Colorectal Cancer ◽  
Non Coding Rnas

scholarly journals Integrated analysis of long non-coding RNAs in human colorectal cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (17) ◽  
pp. 23897-23908 ◽  
Author(s):  
Xiaohua Chen ◽  
Binjian Liu ◽  
Rui Yang ◽  
Yong Guo ◽  
Feng Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Integrated Analysis ◽  
Human Colorectal Cancer ◽  
Non Coding Rnas

scholarly journals Butter: High-precision genomic alignment of small RNA-seq data

2014 ◽  
Author(s):  
Michael J Axtell
Keyword(s):  
Small Rna ◽  
Gene Families ◽  
Superior Performance ◽  
Rna Seq ◽  
Large Numbers ◽  
Genomic Location ◽  
Local Densities ◽  
Gene Regulatory ◽  
Non Coding Rnas ◽  
Specificity Determinants

Eukaryotes produce large numbers of small non-coding RNAs that act as specificity determinants for various gene-regulatory complexes. These include microRNAs (miRNAs), endogenous short interfering RNAs (siRNAs), and Piwi-associated RNAs (piRNAs). These RNAs can be discovered, annotated, and quantified using small RNA-seq, a variant RNA-seq method based on highly parallel sequencing. Alignment to a reference genome is a critical step in analysis of small RNA-seq data. Because of their small size (20-30 nts depending on the organism and sub-type) and tendency to originate from multi-gene families or repetitive regions, reads that align equally well to more than one genomic location are very common. Typical methods to deal with multi-mapped small RNA-seq reads sacrifice either precision or sensitivity. The tool 'butter' balances precision and sensitivity by placing multi-mapped reads using an iterative approach, where the decision between possible locations is dictated by the local densities of more confidently aligned reads. Butter displays superior performance relative to other small RNA-seq aligners. Treatment of multi-mapped small RNA-seq reads has substantial impacts on downstream analyses, including quantification of MIRNA paralogs, and discovery of endogenous siRNA loci. Butter is freely available under a GNU general public license.

scholarly journals Human miRNome Profiling in Colon Adenoma-carcinoma Sequence Reveal Early Deregulation of miR-1246, Which Exhibits Oncogenic Properties in Vitro by Targeting AXIN2 and CFTR

2021 ◽  
Author(s):  
Simonas Juzenas ◽  
Rokas Lukosevicius ◽  
Violeta Salteniene ◽  
Ugne Kulokiene ◽  
Georg Hemmrich-Stanisak ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Western Blot ◽  
Small Rna ◽  
Mirna Expression ◽  
Colony Formation ◽  
Cancer Development ◽  
Luciferase Reporter ◽  
Rna Seq ◽  
Molecular Features

Abstract Background: Regulatory changes occurring early in colorectal cancer development remain poorly investigated. Since the majority of cases develop from polyps in the adenoma-carcinoma pathway, a search of early molecular features, such as aberrations in miRNA expression occurring prior to cancer development, would enable identification of potentially causal, rather than consequential, candidates in the progression of polyp to cancer. This study aim was to discover early miRNA expression changes in adenoma-carcinoma sequence and to investigate the role of deregulated miRNAs in CRC development.Methods: Small RNA-seq data analysis was performed to identify deregulated miRNAs and their isoforms among HC, AP and CRC tissue samples. Deregulated miRNAs were validated using RT-qPCR in the independent patient group. MTT, colony formation and wound healing assays were performed in order to evaluate hsa-miR-1246 function in CRC cells. Luciferase and Western blot assays were used to test hsa-miR-1246 gene targets.Results: In the current study by employing small RNA-seq profiling of colon biopsy samples, we describe differentially expressed miRNAs and their isoforms in the adenoma-carcinoma pathway. Analysis of healthy-adenoma-carcinoma sequence in an independent validation group enabled to identify early deregulated miRNAs including hsa-miR-1246 and hsa-miR-215-5p and up-regulation of hsa-miR-1246 in plasma samples of patients with CRC. Loss-of-function experiments revealed that inhibition of hsa-miR-1246 leads to reduced cell viability, colony formation and migration rate, thereby indicating an oncogenic effect of this miRNA in vitro. Subsequent western blot and luciferase reporter assay provided evidence of hsa-miR-1246 being involved in the regulation of target AXIN2 and CFTR genes’ expression. Conclusions: The present study revealed possible involvement of hsa-miR-1246 in early colorectal cancer development and regulation of tumor suppressors AXIN2 and CFTR.

scholarly journals XBP1 regulates the protumoral function of tumor-associated macrophages in human colorectal cancer

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Yahui Zhao ◽  
Weina Zhang ◽  
Miaomiao Huo ◽  
Peng Wang ◽  
Xianghe Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Endoplasmic Reticulum Stress Response ◽  
Rna Seq ◽  
Human Colorectal Cancer ◽  
Tumor Associated Macrophages ◽  
Unfolded Protein ◽  
Macrophage Phagocytosis ◽  
Potential Strategy ◽  
Protein Response ◽  
Anti Tumor Activity

AbstractMacrophages are among the most abundant immune cells in colorectal cancer (CRC). Re-educating tumor-associated macrophages (TAMs) to switch from protumoral to anti-tumoral activity is an attractive treatment strategy that warrants further investigation. However, little is known about the key pathway that is activated in TAMs. In this study, infitrating CD206+ TAMs in CRC were sorted and subjected to RNA-seq analysis. Differentially expressed genes were found to be enriched in unfolded protein response/endoplasmic reticulum stress response processes, and XBP1 splicing/activation was specifically observed in TAMs. XBP1 activation in TAMs promoted the growth and metastasis of CRC. Ablation of XBP1 inhibited the expression of the pro-tumor cytokine signature of TAMs, including IL-6, VEGFA, and IL-4. Simultaneously, XBP1 depletion could directly inhibit the expression of SIRPα and THBS1, thereby blocking “don’t eat me” recognition signals and enhancing phagocytosis. Therapeutic XBP1 gene editing using AAV2-sgXBP1 enhanced the anti-tumor activity. Together, XBP1 activation in TAMs drives CRC progression by elevating pro-tumor cytokine expression and secretion, as well as inhibiting macrophage phagocytosis. Targeting XBP1 signaling in TAMs may be a potential strategy for CRC therapy.

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