MicroRNAs in the prognosis and therapy of colorectal cancer: From bench to bedside

To, Kenneth Kin Wah; Tong, Christy W.S.; Wu, Mingxia; Cho, William C.

doi:10.3748/wjg.v24.i27.2949

Cited by 166 publications

(148 citation statements)

References 269 publications

(190 reference statements)

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“…Consequently, miRNAs are implicated in the regulation of a series of biological behaviors, including cell proliferation, differentiation, metabolism and carcinogenesis (12). Emerging data have revealed that miRNAs are abnormally expressed in almost every type of human cancer, including NSCLC (13), cervical cancer (14), colorectal cancer (15), prostate cancer (16) and breast cancer (17). miRNAs are closely associated with NSCLC occurrence and development through regulation of multiple malignant behaviors, as either oncogenes or tumor suppressors (18,19).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

et al. 2019

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MicroRNAs (miRNAs/miRs) are frequently differentially expressed in non-small cell lung cancer (NSCLC), and differential miRNAs expression may be closely associated with NSCLC genesis and development. Therefore, an in-depth investigation of the cancer-associated miRNAs that are crucial for NSCLC pathogenesis may provide effective therapeutic targets for patients with this aggressive malignant tumor type. The expression levels and roles of miR-877 have been well studied in hepatocellular carcinoma and renal cell carcinoma. However, the expression pattern and functions of miR-877 in NSCLC as well as associated underlying mechanisms, to the best of our knowledge, have not yet been investigated. The present study revealed that miR-877 expression was downregulated in NSCLC tissues and cell lines. Low miR-877 expression was significantly associated with TNM stage and distant metastasis in patients with NSCLC. Functional experiments demonstrated that recovery of miR-877 expression restricted the proliferation and invasion of NSCLC cells. In addition, bioinformatics analysis predicted insulin-like growth factor 1 receptor (IGF-1R) as a potential target of miR-877. Luciferase reporter assays, reverse transcription-quantitative PCR and western blot analysis further validated that IGF-1R was a direct target of miR-877 in NSCLC. Furthermore, IGF-1R expression was markedly upregulated in NSCLC tissues, and exhibited an inverse correlation with miR-877 expression. Additionally, IGF-1R overexpression reversed the inhibitory effects in NSCLC cells caused by miR-877 upregulation. These findings demonstrated that miR-877 attenuated NSCLC cell proliferation and invasion, at least partly, by downregulating IGF-1R expression, thereby providing an new candidate biomarker for the diagnosis and therapy of patients with NSCLC.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

et al. 2019

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“…Interestingly, when they utilized an antibiotic-treated rat model, all four miRNAs showed lower levels of expression after 6 weeks of antibiotic treatment, but at 2 weeks, half were upregulated and half were downregulated, suggesting a temporal nature to the antibiotic effect on miRNA expression. The potential functional consequences of these changes were not examined and are difficult to predict as let-7b functions as an anti-oncomiRNA (miRNAs that inhibit proto-oncogenes) and miR-141 and miR-200a function as oncomiRNAs in CRC [109][110][111].…”

Section: The Gut Microbiome and Non-coding Rnasmentioning

confidence: 99%

Impact of the gut microbiome on the genome and epigenome of colon epithelial cells: contributions to colorectal cancer development

2019

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In recent years, the number of studies investigating the impact of the gut microbiome in colorectal cancer (CRC) has risen sharply. As a result, we now know that various microbes (and microbial communities) are found more frequently in the stool and mucosa of individuals with CRC than healthy controls, including in the primary tumors themselves, and even in distant metastases. We also know that these microbes induce tumors in various mouse models, but we know little about how they impact colon epithelial cells (CECs) directly, or about how these interactions might lead to modifications at the genetic and epigenetic levels that trigger and propagate tumor growth. Rates of CRC are increasing in younger individuals, and CRC remains the second most frequent cause of cancer-related deaths globally. Hence, a more in-depth understanding of the role that gut microbes play in CRC is needed. Here, we review recent advances in understanding the impact of gut microbes on the genome and epigenome of CECs, as it relates to CRC. Overall, numerous studies in the past few years have definitively shown that gut microbes exert distinct impacts on DNA damage, DNA methylation, chromatin structure and non-coding RNA expression in CECs. Some of the genes and pathways that are altered by gut microbes relate to CRC development, particularly those involved in cell proliferation and WNT signaling. We need to implement more standardized analysis strategies, collate data from multiple studies, and utilize CRC mouse models to better assess these effects, understand their functional relevance, and leverage this information to improve patient care.

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“…miRNAs have been reported to play crucial roles in tumor biological processes, including proliferation, apoptosis, migration, invasion, and differentiation (9). The association of non-coding RNAs especially miRNA dysregulation with the occurrence and development of cancer has been supported by evidence (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-1224-5p Inhibits Metastasis and Epithelial-Mesenchymal Transition in Colorectal Cancer by Targeting SP1-Mediated NF-κB Signaling Pathways

Peng

Yang

et al. 2020

Front. Oncol.

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MicroRNAs (miRNAs) are small non-coding RNAs that play pivotal roles in cancer initiation and progression. However, the roles and molecular mechanisms of miRNAs in colorectal cancer (CRC) progression remain unclear. Here, we show that downregulation of miR-1224-5p in CRC is negatively correlated with SP1 expression and metastasis in patients and xenografted mouse models. Gain-and loss-of-function assays reveal that miR-1224-5p suppresses the migration, invasion, and epithelial-mesenchymal transition (EMT) of CRC cells in vitro and in vivo by directly targeting SP1. Moreover, SP1 promotes the phosphorylation of p65, which results in EMT progress in CRC cells. Clinical analysis reveals that miR-1224-5p and SP1 expression are remarkably associated with advanced clinical features and unfavorable prognosis of patients with CRC. Further study confirms that hypoxia accounts for the depletion of miR-1224-5p in CRC. The enhancement of hypoxia during epithelial-mesenchymal transition and metastasis of CRC cells is abolished by miR-1224-5p. Our findings provide the first evidence that miR-1224-5p is a potential therapeutic target and prognostic biomarker for patients with CRC.

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MicroRNAs in the prognosis and therapy of colorectal cancer: From bench to bedside

Cited by 166 publications

References 269 publications

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

Impact of the gut microbiome on the genome and epigenome of colon epithelial cells: contributions to colorectal cancer development

MicroRNA-1224-5p Inhibits Metastasis and Epithelial-Mesenchymal Transition in Colorectal Cancer by Targeting SP1-Mediated NF-κB Signaling Pathways

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