scholarly journals Expression profiles of circular RNAs in human colorectal cancer based on RNA deep sequencing

2019 ◽  
Vol 33 (7) ◽  
Author(s):  
Jiaxin Ge ◽  
Yanping Jin ◽  
Xueyou Lv ◽  
Qi Liao ◽  
Cong Luo ◽  
...  
2021 ◽  
Vol Volume 14 ◽  
pp. 3821-3832
Author(s):  
Chengzhou Lv ◽  
Wei Sun ◽  
Jiapeng Huang ◽  
Yuan Qin ◽  
Xiaoyu Ji ◽  
...  

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769454 ◽  
Author(s):  
Peili Zhang ◽  
Zhigui Zuo ◽  
Wenjing Shang ◽  
Aihua Wu ◽  
Ruichun Bi ◽  
...  

Circular RNA, a class of non-coding RNA, is a new group of RNAs and is related to tumorigenesis. Circular RNAs are suggested to be ideal candidate biomarkers with potential diagnostic and therapeutic implications. However, little is known about their expression in human colorectal cancer. In our study, differentially expressed circular RNAs were detected using circular RNA array in paired tumor and adjacent non-tumorous tissues from six colorectal cancer patients. Expression levels of selected circular RNAs (hsa_circRNA_103809 and hsa_circRNA_104700) were measured by real-time polymerase chain reaction in 170 paired colorectal cancer samples for validation. Statistical analyses were conducted to investigate the association between hsa_circRNA_103809 and hsa_circRNA_104700 expression levels and respective patient clinicopathological features. Receiver operating characteristic curve was constructed to evaluate the diagnostic values. Our results indicated that there were 125 downregulated and 76 upregulated circular RNAs in colorectal cancer tissues compared with normal tissues. We also first demonstrated that the expression levels of hsa_circRNA_103809 ( p < 0.0001) and hsa_circRNA_104700 ( p = 0.0003) were significantly lower in colorectal cancer than in normal tissues. The expression level of hsa_circRNA_103809 was significantly correlated with lymph node metastasis ( p = 0.021) and tumor-node-metastasis stage ( p = 0.011), and the expression level of hsa_circRNA_104700 was significantly correlated with distal metastasis ( p = 0.036). The area under receiver operating characteristic curves of hsa_circRNA_103809 and hsa_circRNA_104700 were 0.699 ( p < 0.0001) and 0.616 ( p < 0.0001), respectively. In conclusion, these results suggest that hsa_circRNA_103809 and hsa_circRNA_104700 may be potentially involved in the development of colorectal cancer and serve as potential biomarkers for the diagnosis of colorectal cancer.


2013 ◽  
Vol 31 (3) ◽  
pp. 1277-1281 ◽  
Author(s):  
HISAAKI MIYOSHI ◽  
ASAHIRO MORISHITA ◽  
JOJI TANI ◽  
TEPPEI SAKAMOTO ◽  
KOJI FUJITA ◽  
...  

2020 ◽  
Author(s):  
Hong Wang ◽  
David H Wang ◽  
Xu Yang ◽  
Yuhai Sun ◽  
Chung S Yang

Abstract Colitis increases the risk of colorectal cancer; however, the mechanism of the association between colitis and cancer remains largely unknown. To identify colitis-associated cancer promoting factors, we investigated gene expression changes caused by dextran sulfate sodium (DSS)-induced colitis in mice. By analyzing gene expression profiles, we found that IL11 was upregulated in DSS-induced colitis tissue and 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP)/DSS-induced colon tumors in mice as well as in human colorectal cancer. By characterizing the activation/phosphorylation of STAT3 (pSTAT3), we found that pSTAT3 was induced transiently in colitis, but maintained at higher levels from hyper-proliferative dysplastic lesions to tumors. Using the IL11 receptor (IL11Rα1) knockout mice, we found that pSTAT3 in the newly regenerated crypt epithelial cells in colitis is abolished in IL11Rα1+/- and -/- mice, suggesting that colitis-induced IL11 activates STAT3 in colon crypt epithelial cells. Moreover, colitis-promoted colon carcinogenesis was significantly reduced in IL11Rα1+/- and -/- mice. To determine the roles of the IL11 in colitis, we found that the inhibition of IL11 signaling by recombinant IL11 antagonist mutein during colitis was sufficient to attenuate colitis-promoted carcinogenesis. Together, our results demonstrated that colitis-induced IL11 plays critical roles in creating cancer promoting microenvironment to facilitate the development of colon cancer from dormant premalignant cells.


2021 ◽  
Author(s):  
Yansheng Wang ◽  
Baolei Zhang ◽  
Yun Zhu ◽  
Yong Zhang ◽  
Li Li ◽  
...  

Abstract Background: Circular RNAs (circRNAs) have gained wide attention as a class of potential biomarkers for the early detection of multiple cancers. However, the functions and mechanisms of circRNAs in the oncogenesis of human colorectal cancer (CRC) remain to be elucidated. This study aimed to investigate the roles of hsa_circ_0000523 and its parental gene METTL3 in regulating cell proliferation, apoptosis and metastasis in a human CRC cell line (HCT116).Methods: HCT116 cells were left untreated, transfected with hsa_circ_0000523- or METTL3-expressing plasmid, transfected with siRNA oligo against hsa_circ_0000523 or METTL3, or transfected with negative control vector or siRNA oligo. All transfections were performed with Lipofectamine 2000. Transcriptional levels of hsa_circ_0000523, miR-let-7b, and METTL3 were measured by real-time quantitative polymerase chain reaction. Cell proliferation was assessed by CCK-8 assay. Apoptosis was evaluated by flow cytometry after staining for annexin V and propidium iodide. Cellular potential for migration was detected by transwell assay. Results: In HCT116 cells, hsa_circ-0000523 indirectly regulated METTL3 expression by suppressing the transcription of miR-let-7b. The expression of METTL3 promoted cell proliferation and suppressed apoptosis. Higher levels of METTL3 expression were associated with more aggressive tumor invasion.Conclusion: The hsa_circ_0000523/miR-let-7b/METLL3 axis functions in the tumorigenesis and pathogenesis of human CRC. Our results suggest that circRNAs and METTL3 may be used for the highly sensitive diagnosis of CRC and predicting prognosis in patients who have undergone therapy.


2020 ◽  
Author(s):  
Wei Zhang ◽  
Bo Wang ◽  
Yang Yang ◽  
Zhen Zhang ◽  
Quan Wang ◽  
...  

Abstract Background and aim Circular RNAs (circRNAs) have emerged as vital regulators of the initiation and progression of diverse kinds of human cancers. This study aimed to investigate the role of circRNAs in colorectal cancer (CRC). Methods The expression profiles of circRNAs in five pairs of CRC tissues and adjacent normal tissues were analyzed using microarray. Quantitative real-time polymerase chain reaction, in situ hybridization, and BaseScope Assay were used to determine the level and prognostic values of hsa_circ_0000231. Then, in vitro and in vivo functional experiments were performed to investigate the effects of hsa_circ_0000231 on cell proliferation. Mechanistically, fluorescence in situ hybridization, dual-luciferase reporter assay, and RNA pull-down and RNA immunoprecipitation experiments were performed to confirm the interaction between hsa_circ_0000231 and Insulin-like growth factor 2 mRNA-binding protein 3(IGF2BP3) or has_miR-375. Results The expression of hsa_circ_0000231 was upregulated in CRC primary tissues, which indicated poor prognosis of patients with CRC. The results demonstrated that hsa_circ_0000231 could promote CRC cell proliferation as well as tumorigenesis in vitro and in vivo. The mechanistic analysis showed that hsa_circ_0000231 might, on the one hand, act as a competing endogenous RNA of miR-375 to promote cyclin D2 (CCND2) and, on the other hand, bind to the IGF2BP3 protein to prevent CCND2 degradation. Conclusion The findings suggested that hsa_circ_0000231 facilitated CRC progression by sponging miR-375 or binding to IGF2BP3 to modulate CCND2, implying that has_circ_0000231 might be a potential new diagnostic and therapeutic biomarker of CRC.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 3611-3611
Author(s):  
M. Han ◽  
C. T. Liew ◽  
H. W. Zhang ◽  
K. T. Yip ◽  
Z. Y. Song ◽  
...  

3611 Background: Human colorectal cancer (CRC) is the second leading cause of cancer-related death in the United States, and early detection is critical to improve prognosis. To date, we have applied our unique methodology (the Sentinel Principle) to identify blood-based gene expressed biomarkers for several diseases including osteoarthritis, bladder cancer and psychiatric disorders. In the present CRC study, we identified gene signatures from blood cells and characterized a set of biomarkers able to differentiate patients with CRC from controls. Methods: Microarray: 31 blood RNA sample (15 controls; 16 CRC) were profiled using Affymetrix U133Plus2.0 GeneChips. Differentially expressed genes were identified using the non-parametric, Wilcoxon-Mann-Whitney test. SYBR Green real-time RT-PCR: a subset of identified genes was assayed using 115 samples (57 controls; 58 CRC). Logistic regression was used to assess the ability of linear combinations of specific transcripts to distinguish CRC from controls. The diagnostic power for each combination was evaluated by AUC of the Receiver Operating Characteristic (ROC) curve. Blind Test: 83 samples were assayed (45 controls and 38 CRC). Results: Microarray data: 2,779 probes were significantly different in blood gene expression profiles from controls and those from CRC (p<0.05). Real-time RT-PCR: Two up-regulated genes (cytidine deaminase, 1.3 fold with p<0.001; MGC20553 /FERM domain containing 3, 1.2 fold with p=0.031) and three down-regulated genes were validated (B-cell scaffold protein with ankyrin repeats 1, 0.43 fold with p<0.001; B-cell novel protein 1, 0.44 fold with p<0.001; membrane-spanning 4-domains, subfamily A, member 1, 0.44 with p<0.001). Combination analysis: The AUC was 0.883 (95%, C.I. 0.810–0.935) for the best linear combination of these 5 genes. At a cut-off of -1.1, the sensitivity and specificity were 98% and 51%, respectively. Blind Test: The 5-gene set gave sensitivity of 95% (36/38) and specificity of 42% (19/45) with an overall accuracy of 66%. Conclusions: Gene expression signatures from peripheral blood differentiate between CRC patients and controls. The five-gene panel showed high classification performance and could be used as a novel screening tool for CRC. [Table: see text]


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