<i>Retracted:</i> MicroRNA‐431 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the ZEB1‐mediated epithelial–mensenchymal transition

Sun, Kai; Zeng, Tiancai; Huang, Dong; Liu, Zizhong; Huang, Shang; Liu, Jiong; Qu, Zhenfan

doi:10.1016/j.fob.2015.11.001

Cited by 41 publications

(40 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Aberrant expression of certain miRNAs is one of the hallmarks of cancer and can induce the downregulation of tumor suppressive miRNAs or an increase in oncogenic miRNAs that promote cancer development111220. The migration/invasion ability of cancer cells is essential for cancer progression including metastasis leading to cancer-related death.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that miRNAs function as oncogenes or tumor suppressors, and aberrant expression of miRNAs is related to cancer progression via the regulation of cell growth, drug resistance, and metastasis8910. Several reports have demonstrated that miRNAs including miR-431, miR-185-5p, miR-542-5p, and miR-339-5p are involved in the regulation of metastatic cancer cells1112. Although several efforts have been made to control metastasis, the metastatic potential of cancer cells remains largely unknown.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The miR-24-3p/p130Cas: a novel axis regulating the migration and invasion of cancer cells

Kang

Rho

Kim

et al. 2017

Sci Rep

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression by suppressing translation or facilitating mRNA decay. Differential expression of miRNAs is involved in the pathogenesis of several diseases including cancer. Here, we investigated the role of-miR-24-3p as a downregulated miRNA in metastatic cancer. miR-24-3p was decreased in metastatic cancer and lower expression of miR-24-3p was related to poor survival of cancer patients. Consistently, ectopic expression of miR-24-3p suppressed the cell migration, invasion, and proliferation of MCF7, Hep3B, B16F10, SK-Hep1, and PC-3 cells by directly targeting p130Cas. Stable expression of p130Cas restored miR-24-3p-mediated inhibition of cell migration and invasion. These results suggest that miR-24-3p functions as a tumor suppressor and the miR-24-3p/p130Cas axis is a novel factor of cancer progression by regulating cell migration and invasion.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The miR-24-3p/p130Cas: a novel axis regulating the migration and invasion of cancer cells

Kang

Rho

Kim

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…ZEB1 has been shown to be a molecular target of miR‐431 in human lung adenocarcinoma and hepatocellular carcinoma . We found that in ACC H295R cells, ZEB1 mRNA transcript (Fig.…”

Section: Resultsmentioning

confidence: 69%

microRNA-431 as a Chemosensitizer and Potentiator of Drug Activity in Adrenocortical Carcinoma

et al. 2019

View full text Add to dashboard Cite

Background Adrenocortical carcinoma (ACC) is a rare endocrine cancer with treatments limited in efficacy for metastatic disease. New molecular targeted therapies have yet to improve patient outcomes. In contrast, established treatment regimens of adrenolytics and chemotherapy have demonstrated treatment benefit, although admittedly in a minority of patients. Identification of microRNAs (miRNAs) in patients responsive to adjuvant therapy may offer a means to sensitize patients with progressive disease to existing adjuvant regimens. Materials and Methods Samples from primary ACC tumors of 10 Stage IV patients were examined for differentially expressed miRNAs between a “sensitive” and “resistant” cohort. Candidate microRNAs were restored via transfection in two functional ACC cell lines. Gain of function and effects on apoptosis and cell cycle were assessed. Results microRNA‐431 (miR‐431) was underexpressed in patients with ACC with progressive disease undergoing adjuvant therapy. Restoration of miR‐431 in vitro decreased the half maximal inhibitory concentrations of doxorubicin and mitotane, with markedly increased apoptosis. We found that a reversal of epithelial‐mesenchymal transition underlies the action of miR‐431 with doxorubicin treatment, with Zinc Finger E‐Box Binding Homeobox 1 implicated as the molecular target of miR‐431 in ACC. Conclusion This is the first report of the potential of miRNA therapy to sensitize ACC to current established adjuvant therapy regimens, which may mitigate the resistance underlying treatment failure in patients with advanced ACC. Effective and well‐studied methods of targeted miRNA delivery in existence hints at the imminent translatability of these findings. Implications for Practice Adrenocortical carcinoma (ACC) is a rare endocrine cancer with outcomes not improving despite extensive research and new targeted therapies. Mitotane and etoposide/doxorubicin/cisplatin chemotherapy is trial validated for improved recurrence‐free survival. However, a minority of patients experience sustained benefit. Significant side effects exist for this regimen, with patients often unable to attain target drug doses shown to give survival benefit. This preclinical study examines the role of microRNAs in sensitizing ACC to doxorubicin or mitotane. This study offers an important bridge between new and existing cancer treatments, offering an imminently translatable approach to the treatment of adrenocortical carcinoma.

show abstract

“…To explore the possible mechanism through which rs112395617 is involved in HCC susceptibility, miRNAs that would be able to bind with the JAK1 3' UTR and be affected by rs112395617 were predicted, and it was identified that miR-431-5p was able to bind with the del/del genotype, but not the ins/ins genotype, and consequently down regulated the expression of JAK1, thus reducing the risk of HCC. miR-431, formerly hypothesized to be a nervous system-specific miRNA (29), has been identified to have a role as a novel tumor-related miRNA (30)(31)(32)(33). Elevated expression of miR-431 was demonstrated to be able to act as a biomarker in differentiating patients with colorectal cancer (CRC) from healthy controls (30), suggesting an oncogenic role in CRC.…”

Section: Discussionmentioning

confidence: 99%

An indel polymorphism in the 3' untranslated region of JAK1 confers risk for hepatocellular carcinoma possibly by regulating JAK1 transcriptional activity in a Chinese population

Qian

Wang

et al. 2018

Oncol Lett

View full text Add to dashboard Cite

The purpose of the present study was to assess whether the rs112395617 polymorphism located in the Janus kinase 1 () 3' untranslated region (3' UTR) was associated with the risk of hepatocellular carcinoma (HCC), and to explore the potential mechanism of action. Genomic DNA was extracted from peripheral blood of 290 patients with HCC and 320 controls. A polymerase chain reaction-polyacrylamide gel electrophoresis assay was used to genotype the rs112395617 polymorphism. Quantitative (q)PCR was used to detect the genotype-phenotype association between HCC tissues and different genotypes. Vectors containing the insertion (ins)/ins or deletion (del)/del genotype of the rs112395617 polymorphism were constructed, and the luciferase assay was used to detect the transcriptional activity affected by the rs112395617 polymorphism. It was identified that, when compared with the ins/ins genotype, the del/del and del/ins genotypes of rs112395617 were significantly associated with a decreased risk of HCC. The qPCR results demonstrated that the mRNA expression level with ins/ins and ins/del genotypes was increased by 3.36 and 1.75-fold compared with the del/del genotype in human HCC tissue samples. In addition, the 'AATT' insertion allele of rs112395617 disrupted the binding site for microRNA (miR)-431-5p, thereby increasing transcription. These data suggest that the rs112395617 polymorphism may contribute to HCC susceptibility, in full or at least partially through an effect on transcriptional activity by disrupting its binding with miR-431-5p.

show abstract

Retracted: MicroRNA‐431 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the ZEB1‐mediated epithelial–mensenchymal transition

Cited by 41 publications

References 25 publications

The miR-24-3p/p130Cas: a novel axis regulating the migration and invasion of cancer cells

The miR-24-3p/p130Cas: a novel axis regulating the migration and invasion of cancer cells

microRNA-431 as a Chemosensitizer and Potentiator of Drug Activity in Adrenocortical Carcinoma

An indel polymorphism in the 3' untranslated region of JAK1 confers risk for hepatocellular carcinoma possibly by regulating JAK1 transcriptional activity in a Chinese population

Contact Info

Product

Resources

About