LncRNAs: Potential Novel Prognostic and Diagnostic Biomarkers in Colorectal Cancer

Dastmalchi, Narges; Safaralizadeh, Reza; Nargesi, Mirsaed Miri

doi:10.2174/0929867326666190227230024

Cited by 42 publications

(26 citation statements)

References 75 publications

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“…Long non‐coding RNAs (lncRNAs) are well‐established mediators that play critical roles in various cellular pathways 6 . It is reported that X‐inactivation‐specific transcript (XIST) is a lncRNA as an indicator of many human tumours 7 .…”

Section: Introductionmentioning

confidence: 99%

The crosstalk network of XIST/miR‐424‐5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer

Deng

Jin

et al. 2021

Liver International

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Background Liver cancer is a major public health concern, but the mechanistic actions of biomarkers contributing to liver cancer remain to be determined. In this study, we aimed to investigate the regulatory cascade of microRNA‐424‐5p (miR‐424‐5p), X‐inactive‐specific transcript (XIST) and O‐GlcNAc transferase (OGT) in liver cancer. Methods Differentially expressed miRNAs and target genes related to liver cancer were predicted by bioinformatics analyses, and their expression was determined in liver tissues of patients with liver cancer and liver cancer cells. The RNA immunoprecipitation (RIP), RNA pull‐down and dual luciferase reporter assay were used to examine the binding affinity among XIST and miR‐424‐5p and OGT. Then, gain‐ and loss‐of‐function assays were conducted to evaluate the effects of the XIST/miR‐424‐5p/OGT axis on malignant phenotypes. A nude mouse model of liver cancer was further established for in vivo substantiation. Results XIST and OGT were up‐regulated in liver cancer tissues and cells, responsible for poor prognosis in patients with liver cancer, while miR‐424‐5p was down‐regulated. XIST competitively bound to miR‐424‐5p to increase OGT expression. XIST silencing inhibited malignant phenotypes of liver cancer cells, while miR‐424‐5p down‐regulation negated its effect. miR‐424‐5p suppressed RAF1 glycosylation by negatively regulating OGT expression and promoted its ubiquitination/degradation. Furthermore, XIST knockdown inhibited tumour growth and metastasis in nude mice, while ectopic OGT reversed its effect. Conclusion These results reveal a novel mechanism by which the interaction of XIST/miR‐424‐5p/OGT participates in the malignancy and metastasis of liver cancer.

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Section: Introductionmentioning

confidence: 99%

The crosstalk network of XIST/miR‐424‐5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer

Deng

Jin

et al. 2021

Liver International

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“…Although the mode and regulatory mechanism of lncRNAs in tumors have not been thoroughly studied, lncRNAs are verified to play a vital role in the occurrence and development of human cancers [ 5 ]. At present, it has been found that related lncRNAs are involved in the occurrence, metastasis and invasion, early diagnosis, prognosis evaluation, and radiotherapy and chemotherapy efficacy of CRC [ 6 , 7 ]. LncNEAT1 was reported to promote CRC progression by suppressing miR-486-5p expression and regulating NR4A1/Wnt/ β -catenin pathway [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA MSC-AS1 Promotes Colorectal Cancer Progression by Regulating miR-325/TRIM14 Axis

Wang

et al. 2021

Journal of Oncology

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Background. LncRNA MSC-AS1 has been reported to be a tumor promoter in hepatocellular carcinoma. However, the function of MSC-AS1 in colorectal cancer (CRC) has not been elucidated. It is designed to study the expression level of MSC-AS1 and investigate its biological effect on the progression of CRC. Methods. The expression patterns of MSC-AS1, miR-325, and TRIM14 were explored by RT-qPCR in CRC tissues and cells. The protein expression of TRIM14 was tested by Western blot assay. The association between MSC-AS1 expression and clinicopathological data was analyzed by chi-squared test. CCK-8 assay, colony formation, and Transwell assay were used to investigate the effect of MSC-AS1 on cell growth, invasion, and migration in CRC cells. The correlations among MSC-AS1, miR-325, and TRIM14 were analyzed by Pearson’s correlation coefficient analysis. Results. We found that MSC-AS1 and TRIM14 were upregulated in CRC tissues, while miR-325 was downregulated in CRC tissues. Functional experiments demonstrated that MSC-AS1 knockdown inhibited cell proliferation, migration, and invasion abilities in CRC cells. Additionally, miR-325 was proved to be a target miRNA of MSC-AS1, and TRIM14 might be a downstream gene of miR-325. Besides that, MSC-AS1 counteracted the inhibitory effect of miR-325 on the cell progression and TRIM14 expression. Conclusion. Our results indicated that MSC-AS1 facilitated CRC progression by sponging miR-325 to upregulate TRIM14 expression. We suggested that MSC-AS1 might be a potential lncRNA-target for CRC therapy.

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“…LncRNAs affect critical CRC signaling pathways by acting both as oncogenes and tumor suppressors through interactions with other regulatory molecules (13)(14)(15). Several lncRNAs have been reported to be dysregulated in CRC, suggesting promising potentiality for theranostic applications (16)(17)(18). However, the molecular mechanisms of action in CRC pathobiology were elucidated only for few of them, such as, CCAT1, CCAT2, H19, HOTAIR, MALAT1, and UCA1 (19)(20)(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

LINC00483 Has a Potential Tumor-Suppressor Role in Colorectal Cancer Through Multiple Molecular Axes

et al. 2021

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Long non-coding RNAs (lncRNAs) are the most heterogeneous class of non-protein-coding RNAs involved in a broad spectrum of molecular mechanisms controlling genome function, including the generation of complex networks of RNA-RNA competitive interactions. Accordingly, their dysregulation contributes to the onset of many tumors, including colorectal cancer (CRC). Through a combination of in silico approaches (statistical screening of expression datasets) and in vitro analyses (enforced expression, artificial inhibition, or activation of pathways), we identified LINC00483 as a potential tumor suppressor lncRNA in CRC. LINC00483 was downregulated in CRC biopsies and metastases and its decreased levels were associated with severe clinical features. Inhibition of the MAPK pathway and cell cycle arrest by starvation induced an upregulation of LINC00483, while the epithelial to mesenchymal transition activation by TGFβ-1 and IL-6 caused its down-modulation. Moreover, enforced expression of LINC00483 provoked a slowing down of cell migration rate without affecting cell proliferation. Since LINC00483 was predominantly cytoplasmic, we hypothesized a “miRNA sponge” role for it. Accordingly, we computationally reconstructed the LINC00483/miRNA/mRNA axes and evaluated the expression of mRNAs in different experimental conditions inducing LINC00483 alteration. By this approach, we identified a set of mRNAs sharing the miRNA response elements with LINC00483 and modulated in accordance with it. Moreover, we found that LINC00483 is potentially under negative control of transcription factor HNF4α. In conclusion, we propose that LINC00483 is a tumor suppressor in CRC that, through an RNA-RNA network, may control cell migration and participate in proliferation signaling.

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LncRNAs: Potential Novel Prognostic and Diagnostic Biomarkers in Colorectal Cancer

Cited by 42 publications

References 75 publications

The crosstalk network of XIST/miR‐424‐5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer

The crosstalk network of XIST/miR‐424‐5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer

LncRNA MSC-AS1 Promotes Colorectal Cancer Progression by Regulating miR-325/TRIM14 Axis

LINC00483 Has a Potential Tumor-Suppressor Role in Colorectal Cancer Through Multiple Molecular Axes

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