scholarly journals LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Yihao Zhu ◽  
Hanqing Hu ◽  
Ziming Yuan ◽  
Qian Zhang ◽  
Huan Xiong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chromatin Remodeling ◽  
Chromatin Immunoprecipitation ◽  
Cancer Stemness ◽  
Functional Studies ◽  
Non Coding Rna ◽  
New Strategy ◽  
Lncrna Neat1 ◽  
Long Non Coding Rna

Abstract Resistance of chemotherapy is one of causes of recurrence and poor prognosis in patients with colorectal cancer (CRC). The role of differentially expressed long non-coding RNA (lncRNA) in 5-fluorouracil (5-Fu) resistance has not been fully elucidated. Here we observed that lncRNA NEAT1 was associated with 5-Fu resistance in CRC. Our Functional studies showed that NEAT1 promoted 5-Fu resistance in colorectal cells. In addition, A-TAC sequencing and chromatin immunoprecipitation (ChIP) showed that NEAT1 affected chromatin remodeling, increased the acetylation levels of histones, increased their enrichment at the promoters of ALDH1 and c-Myc, and promoted the expression of ALDH1 and c-Myc. Taken together, our study suggested that NEAT1 promoted 5-Fu resistance and cancer stemness by remodeling chromatin. Our finding provides a novel role of NEAT1 and may provide a new strategy for the treatment of CRC 5-Fu resistance.

scholarly journals MIR600HG suppresses metastasis and enhances oxaliplatin chemosensitivity by targeting ALDH1A3 in colorectal cancer

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Yi Yao ◽  
Nan Li
Keyword(s):  
Colorectal Cancer ◽  
Animal Experiments ◽  
Experimental Studies ◽  
Non Coding Rna ◽  
Tumour Formation ◽  
Cell Metastasis ◽  
New Strategy ◽  
Long Non Coding Rna ◽  
Normal Controls

Abstract Background: Metastasis and chemoresistance indicate a poor prognosis in colorectal cancer (CRC) patients. However, the mechanisms that lead to the development of chemoresistance and metastasis in CRC remain unclear. Materials and methods: We combined clinical and experimental studies to determine the role of MIR600HG in CRC metastasis and chemoresistance. The statistical analysis was performed using GraphPad Prism software, version 8.0. Results: We detected down-regulated expression of long non-coding RNA (lncRNA) MIR600HG in CRC specimens and cell lines compared with normal controls, and the expression level of MIR600HG was inversely correlated with the overall survival of CRC patients. The inhibition of MIR600HG stimulated CRC cell metastasis and chemoresistance. In addition, our data showed that the inhibition of MIR600HG stimulated CRC stemness, while the overexpression of MIR600HG suppressed stemness. Importantly, our animal experiments showed that MIR600HG inhibited tumour formation and that the combination of MIR600HG inhibition and oxaliplatin (Oxa) treatment significantly inhibited tumour growth compared with that with either intervention alone. Furthermore, we demonstrated that MIR600HG exerts its anticancer role by targeting ALDH1A3 in CRC. Conclusions: Our data suggest that MIR600HG functions as a tumour suppressor and that the overexpression of MIR600HG inhibits tumour invasion and enhances chemosensitivity, providing a new strategy for CRC treatment.

scholarly journals Long Non-coding RNA MAFG-AS1 Promotes Cell Proliferation, Migration, and EMT by miR-3196/STRN4 in Drug-Resistant Cells of Liver Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Tianming Chen ◽  
Bin Huang ◽  
Yaozhen Pan
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistant ◽  
Non Coding Rna ◽  
Different Types ◽  
Non Coding Rnas ◽  
Novel Target ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Resistant Cells

Long non-coding RNAs (lncRNAs) have been shown to participate in the development and progression of several different types of cancer. Past studies indicated that lncRNA MAFG-antisense 1 (AS1) promotes colorectal cancer. However, the role of MAFG-AS1 in hepatocellular carcinoma (HCC) remains unclear. The aim of the present study is to examine the effect of lncRNA MAFG-AS1 on drug resistance HCC. The results indicated that MAFG-AS1 is upregulated in drug-resistant cells. Further, MAFG-AS1 promotes growth and migration of HCC by upregulating STRN4 through absorbing miR-3196. Thus, LncRNA MAFA-AS1 may become a novel target to treat HCC patients.

scholarly journals Genome-wide analysis of long non-coding RNA expression and function in colorectal cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770365 ◽  
Author(s):  
Fangyuan Jing ◽  
Huicheng Jin ◽  
Yingying Mao ◽  
Yingjun Li ◽  
Ye Ding ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Expression Profile ◽  
Colorectal Carcinogenesis ◽  
Rna Expression ◽  
Rna Transcripts ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Long non-coding RNAs (lncRNAs) are widely transcribed in the genome, but their expression profile and roles in colorectal cancer are not well understood. The aim of this study was to investigate the long non-coding RNA expression profile in colorectal cancer and look for potential diagnostic biomarkers of colorectal cancer. Long non-coding RNA microarray was applied to investigate the global long non-coding RNA expression profile in colorectal cancer. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed using standard enrichment computational methods. The expression levels of selected long non-coding RNAs were validated by quantitative reverse transcription polymerase chain reaction. The relationship between long non-coding RNA expression levels and clinicopathological characteristics of colorectal cancer patients was assessed. Coexpression analyses were carried out to find the coexpressed genes of differentially expressed long non-coding RNAs, followed by gene ontology analysis to predict the possible role of the selected long non-coding RNAs in colorectal carcinogenesis. In this study, a total of 1596 long non-coding RNA transcripts and 1866 messenger RNA transcripts were dysregulated in tumor tissues compared with paired normal tissues. The top upregulated long non-coding RNAs in tumor tissues were CCAT1, UCA1, RP5-881L22.5, NOS2P3, and BC005081 and the top downregulated long non-coding RNAs were AK055386, AC078941.1, RP4-800J21.3, RP11-628E19.3, and RP11-384P7.7. Long non-coding RNA UCA1 was significantly upregulated in colon cancer, and AK055386 was significantly downregulated in tumor with dimension <5 cm. Functional prediction analyses showed that both the long non-coding RNAs coexpress with cell cycle related messenger RNAs. The current long non-coding RNA study provided novel insights into expression profile in colorectal cancer and predicted the potential roles of long non-coding RNAs in colorectal carcinogenesis. Among the dysregulated long non-coding RNAs, UCA1 was found to be associated with anatomic site, and AK055386 was found associated with tumor size. Further functional investigations into the molecular mechanisms are warranted to clarify the role of long non-coding RNA in colorectal carcinogenesis.

scholarly journals Functional role of long non-coding RNA CASC19/miR-140-5p/CEMIP axis in colorectal cancer progressionin vitro

2019 ◽  
Vol 25 (14) ◽  
pp. 1697-1714 ◽  
Author(s):  
Xiao-Dong Wang ◽  
Jian Lu ◽  
Yun-Shou Lin ◽  
Chao Gao ◽  
Feng Qi
Keyword(s):  
Colorectal Cancer ◽  
Functional Role ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals SNHG7 has an oncogenic role in colorectal cancer via potential sponging of MIR-485-5P and MIR-193A-5P; in silico approach

Genetika ◽  
2021 ◽  
Vol 53 (1) ◽  
pp. 65-78
Author(s):  
Farinaz Ziaee ◽  
Mohammadreza Hajjari ◽  
Seyed Kazeminezhad ◽  
Mehrdad Behmanesh
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
In Silico ◽  
Potential Role ◽  
Non Coding Rna ◽  
In Silico Study ◽  
Competing Endogenous Rnas ◽  
Long Non Coding Rna ◽  
In Silico Analyses

SNHG7, as a member of the small nucleolar host gene family, is a recently identified long non-coding RNA (lncRNA). Different reports have identified the SNHGs as competing endogenous RNAs (ceRNAs) sponging miRNAs with a role in cancer progression. However, the biological functions of SNHG7 in the colorectal cancer (CRC) remained to be almost unknown. The current in silico study was aimed to find the potential role of SNHG7 in the CRC development. In this study, we showed the up-regulation of SNHG7 as well as its potential correlation with miRNAs, including mir-193a-5p and mir-485-5P. We hypothesized that SNHG7 modulates these miRNAs availability by acting as a molecular sponge. Our findings showed the potential targets of these miRNAs by studying different databases as well as in silico analyses. In summary, we found SNHG7 as a potential ceRNA which may be a promising biomarker for diagnostic and therapeutic target in CRC.

scholarly journals Long Non-Coding RNA CBR3-AS1 Promotes Stem-Like Properties and Oxaliplatin Resistance of Colorectal Cancer by Sponging miR-145-5p

2020 ◽  
Author(s):  
Liangbao Xie ◽  
Guangfei Cui ◽  
Tao Li
Keyword(s):  
Colorectal Cancer ◽  
Direct Interaction ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
Mammosphere Formation ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

Abstract Background: Accumulating evidence has shown that long non-coding RNAs (lncRNAs) serve as essential regulators in a plethora of human cancers. In this study, we analyzed the expression profile and functional role of lncRNA CBR3-AS1 in colorectal cancer (CRC).Methods: CRC tissues and paired adjacent normal tissues were obtained from 133 patients. The expression levels of CBR3-AS1 and miR-145-5p in tissues and cells were detected by RT-qPCR analysis. The proliferation, oxaliplatin resistance, apoptosis, migration, invasion and stem-like properties of CRC cells were detected by MTT assay, flow cytometry analysis, transwell assay and mammosphere formation assay, respectively. Western blot analysis was performed to detect the expression levels of relevant proteins. Dual-luciferase reporter assay and RNA immunoprecipitation assay verified the direct interaction between CBR3-AS1 and miR-145-5p in CRC.Results: High expression levels of CBR3-AS1 were found in CRC tissues and cell lines. Upregulated CBR3-AS1 was closely associated with poor prognosis and adverse clinicopathological features of CRC patients. Artificial knockdown of CBR3-AS1 markedly suppressed the proliferation, migration, invasion and stem-like properties, but promoted the apoptosis of CRC cells. Moreover, we observed that CBR3-AS1 could directly bind to miR-145-5p and negatively regulated its expression in CRC. Further experiments also demonstrated that inhibition of miR-145-5p reverted the effects of CBR3-AS1 knockdown on CRC cells. In addition, compared with the parental cells, CBR3-AS1 expression was strikingly increased in oxaliplatin-resistant CRC cells, and the oxaliplatin resistance was notably diminished by CBR3-AS1 knockdown. Conclusions: To conclude, our study suggested that CBR3-AS1 serves an oncogenic role in CRC, and may be exploited as a novel therapeutic target for CRC patients.

scholarly journals Long non-coding RNA SNHG16 affects cell proliferation and predicts a poor prognosis in patients with colorectal cancer via sponging miR-200a-3p

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Yanling Li ◽  
Ying Lu ◽  
Yanglong Chen
Keyword(s):  
Colorectal Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Non Coding Rna ◽  
Promote Tumor Growth ◽  
Cell Growth And Proliferation ◽  
Long Non Coding Rna

Abstract Previous study has explored that SNHG16, a long non-coding RNA (lncRNA), mediated cell growth and proliferation. Yet, the role of SNHG16 in human colorectal cancer (CRC) still remains to be explored. Therefore, we conducted the present study to explore the functions of SNHG16 in CRC. In the present study, SNHG16 was significantly up-regulated in CRC tissues and cell lines. Gain- and loss-of-function of SNHG16 further presented that SNHG16 promoted the progression of CRC cells, including proliferation, migration, and invasion. Further, in vivo study also revealed that overexpression of SNHG16 could promote tumor growth. Bioinformatics analysis and luciferase reporter assay showed that SNHG16 was a direct target of miR-200a-3p. MiR-200a-3p was inversely correlated with SNHG16 expression in CRC tissues. In brief, the above results elucidate the important role of SNHG16 in CRC tumorigenesis, suggesting that SNHG16 might be quite vital for the diagnosis and development of CRC.

The lncRNA TUG1 promotes cell growth and migration via the TUG1/miR-145-5p/TRPC6 pathway in colorectal cancer

2020 ◽  
Author(s):  
Xiaoqiang Wang ◽  
Xiaomin Bai ◽  
Zhonghui Yan ◽  
Xinyu Guo ◽  
Youcheng Zhang
Keyword(s):  
Colorectal Cancer ◽  
Underlying Mechanism ◽  
Clinical Samples ◽  
Cell Growth And Migration ◽  
Cellular Processes ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Taurine Upregulated Gene 1

Colorectal cancer (CRC) is the third most prevalent malignant tumor. Taurine upregulated gene 1 (TUG1), a long non-coding RNA (lncRNA), has been shown to be involved in the physiological and pathological processes of CRC. However, the role of TUG1 in the progression of CRC and its underlying mechanism are largely unknown. Here, we measured TUG1 expression in clinical samples from CRC patients and found that TUG1 expression was higher in CRC tissues as compared to that in normal adjacent tissues. We then inhibited TUG1 with siRNAs in two CRC cell lines and found that TUG1 knockdown inhibited the viability, proliferation, and migration of CRC cells and lowered the ability of CRC cells to form subcutaneous tumors. Furthermore, we revealed that TUG1 affected the cellular processes in CRC cells by sponging miR-145-5p. We further found that miR-145-5p inhibited TRPC6 expression, and overexpression of TRPC6 restored the role of miR-145-5p in CRC cells. Collectively, we illustrated that TUG1 manifests its functions by modulating the TUG1/miR-145-5p/TRPC6 regulatory axis. In conclusion, our study revealed a novel molecular mechanism of TUG1 in CRC progression and suggested the potential of the TUG1/miR-145-5p/TRPC6 pathway to serve as a target for the diagnosis and treatment of CRC.

scholarly journals Long non-coding RNA Lnc-LALC facilitates colorectal cancer liver metastasis via epigenetically silencing LZTS1

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Chuan Zhang ◽  
Lu Wang ◽  
Chi Jin ◽  
Jiahui Zhou ◽  
Chaofan Peng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Liver Metastasis ◽  
Malignant Tumors ◽  
Methylation Status ◽  
Dna Methyltransferases ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractColorectal cancer (CRC) is one of the most common cancers around the world and endangers human health seriously. Liver metastasis is an important factor affecting the long-term prognosis of CRC and the specific mechanism of CRLM (colorectal cancer with liver metastasis) is not fully understood. LZTS1 has been found dysregulated in many cancers, especially in CRC. Theories suggested that hypermethylation of the promoter regions of LZTS1 was responsible for LZTS1 abnormal expression in multiple malignant tumors. Although the role of LZTS1 in CRC cell proliferation has been reported, its role in CRLM remains unclear. Numerous studies reported Long non-coding RNA (lncRNA) could regulate the gene expression level by regulating gene methylation status in many tumors. However, whether there were lncRNAs could change the methylation status of LZTS1 or not in CRLM was unknown. In this study, we aimed to investigate whether there are lncRNAs can regulate the expression of LZTS1 through affecting DNA methylation in CRLM. We found that upregulated Lnc-LALC in CRC was negatively correlated with LZTS1 expression, and Lnc-LALC could regulate LZTS1 expression in both mRNA and protein level in our study. Functionally, Lnc-LALC enhanced the CRC cells metastasis ability in vitro and vivo through inhibiting the expression of LZTS1. Furthermore, the precise mechanisms exploration showed that lnc-LALC could recruit DNA methyltransferases (DNMTs) to the LZTS1 promoter by combining with Enhancer of zeste homolog 2(EZH2) and then altered the expression of LZTS1 via DNMTs-mediated DNA methylation. Collectively, our data demonstrated the important role of Lnc-LALC/ LZTS1 axis in CRLM development.

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