Epithelial-mesenchymal transition-associated microRNAs in colorectal cancer and drug-targeted therapies (Review)

Jin, Danjuan; Fang, Yantian; Li, Zhengyang; Chen, Zongyou; Xiang, Jianbin

doi:10.3892/or.2014.3638

Cited by 24 publications

(17 citation statements)

References 154 publications

(141 reference statements)

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“…EMT evens are central to tumor progression and malignant transformation in CRC [8]. Accordingly, further studies were performed to confirm whether miR-489 regulated EMT process of CRC cells.…”

Section: Resultsmentioning

confidence: 99%

“…TWIST1 plays an essential role in tumor metastasis including CRC [6, 7]. TWIST1 leads to loss of E-cadherin-mediated cell-cell adhesion, increased expression of mesenchymal markers, and induction of cell motility in CRC cells [6, 8]. Recent study reported that miR-381 inhibited migration, invasion and EMT of CRC cells by targeting TWIST1 [9].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

et al. 2017

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microRNA-489 (miR-489) is a novel cancer-related miRNAs and functions as a tumor suppressor in human cancers. While, the clinical significance of miR-489 and its role in colorectal cancer (CRC) remain rarely known. Here, we found that the levels of miR-489 in CRC tissues were significantly lower than those in matched tumor-adjacent tissues. Furthermore, decreased levels of miR-489 also observed in CRC cell lines compared to HIEC cells. Clinicopathological analysis revealed that miR-489 underexpression was positively correlated with advanced pT stage, pN stage and AJCC stage. Moreover, miR-489 low expressing CRC patients showed a obvious shorter survival. Functionally, miR-489 restoration inhibited cell migration and invasion as well as epithelial-mesenchymal transition (EMT) in HCT116 cells, while miR-489 loss facilitated these cellular processes in SW480 cells. In vivo experiments revealed that miR-489 overexpression reduced the number of metastatic nodules in nude mice liver. Notably, TWIST1 was recognized as a direct downstream target of miR-489 in CRC cells. Interestingly, TWIST1 restoration abrogated the effects of miR-489 on CRC cells with enhanced cell migration, invasion and EMT process. Furthermore, overexpression of long noncoding RNA cardiac hypertrophy-related factor (lncRNA CHRF) was inversely correlated with miR-489 expression in CRC tissues. CHRF knockdown increased the expression of miR-489 and suppressed EMT events of HCT116 cells, while CHRF overexpression showed opposite effects on miR-489 expression and EMT in SW480 cells. Taken together, this work support the first evidence that lncRNA CHRF-induced miR-489 loss facilitates metastasis and EMT process of CRC cells probably via TWIST1/EMT signaling pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

et al. 2017

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“…The first one is upregulated by the EMT inducer Snail that causes the opposite effect on miR-203. miR-200a and miR-200c are also downregulated in CSCs, allowing the expression of EMT inducers Zeb1 and Zeb2 with a concomitant decrease in E-cadherin levels and increased expression of stem cell markers CD166 and CD133 [162]. Other miRNAs have been described as important for the maintenance of the cancer stem cell phenotype.…”

Section: Noncoding Rnas and Their Involvement In Colorectal Cancermentioning

confidence: 99%

Colorectal Cancer: From the Genetic Model to Posttranscriptional Regulation by Noncoding RNAs

Lizarbe

Calle-Espinosa

Fernández-Lizarbe

et al. 2017

BioMed Research International

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Colorectal cancer is the third most common form of cancer in developed countries and, despite the improvements achieved in its treatment options, remains as one of the main causes of cancer-related death. In this review, we first focus on colorectal carcinogenesis and on the genetic and epigenetic alterations involved. In addition, noncoding RNAs have been shown to be important regulators of gene expression. We present a general overview of what is known about these molecules and their role and dysregulation in cancer, with a special focus on the biogenesis, characteristics, and function of microRNAs. These molecules are important regulators of carcinogenesis, progression, invasion, angiogenesis, and metastases in cancer, including colorectal cancer. For this reason, miRNAs can be used as potential biomarkers for diagnosis, prognosis, and efficacy of chemotherapeutic treatments, or even as therapeutic agents, or as targets by themselves. Thus, this review highlights the importance of miRNAs in the development, progression, diagnosis, and therapy of colorectal cancer and summarizes current therapeutic approaches for the treatment of colorectal cancer.

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“…MicroRNAs (miRNAs) are a class of small, non-coding RNAs of 19 to 24 nucleotides that post-transcriptionally regulate gene expression through RNA interference, gene silencing pathways [4][5][6][7][8][9][10]. Presently, 1881 precursors and 2588 mature miRNAs in human have been identified by the latest version of miRBase (v.21, http://www.mirbase.org/ on 24th, January, 2016) [11].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive investigation of aberrant microRNA profiling in bladder cancer tissues

Wei

et al. 2016

Tumor Biol.

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There has been accumulative evidence that microRNAs (miRNAs) play essential roles in the tumorigenesis and progression of bladder cancer. However, individual studies and small sample size caused discrepant outcomes. Thus, the current study focused on a comprehensive profiling of all differentially expressed miRNAs in a total of 519 bladder cancer tissue samples, based on miRNA microarray data. Altogether, 11 prioritized miRNAs stated by 21 published microarray datasets, including five down-regulated (miR-133a-3p, miR-1-3p, miR-99a-5p, miR-490-5p, and miR-133b) and six up-regulated candidate miRNAs (miR-182-5p, miR-935, miR-518e-3p, miR-573, miR-100-3p, and miR-3171) were analyzed with vote-counting strategy and a Robust Rank Aggregation method. Subsequently, miRNA in silico target prediction and potential pathway enrichment analysis were performed to investigate the prospective molecular mechanism of miRNAs in the tumorigenesis of bladder cancer. We found that most of the relative pathways of the aberrantly expressed miRNAs found in the current study were closely correlated with different biological processes, cellular components, molecular functions, cancer pathogeneses, and some cell signalings, such as Wnt signaling, insulin/IGF, PI3 kinase, and FGF signaling pathways. Hence, a comprehensive overview on the miRNA expression pattern in bladder cancer tissues was gained by the current study. These miRNAs might be involved in the tumorigenesis and deterioration of bladder cancer.

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Epithelial-mesenchymal transition-associated microRNAs in colorectal cancer and drug-targeted therapies (Review)

Cited by 24 publications

References 154 publications

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway

Colorectal Cancer: From the Genetic Model to Posttranscriptional Regulation by Noncoding RNAs

Comprehensive investigation of aberrant microRNA profiling in bladder cancer tissues

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