miR‐204‐5p suppresses hepatocellular cancer proliferation by regulating homeoprotein <scp>SIX</scp>1 expression

Chu, Yi; Jiang, Mingzuo; Du, Feng; Chen, Di; Tao, Ye; Xu, Bing; Li, Xiaowei; Wang, Weijie; Qiu, Zhaoyan; Liu, Haiming; Nie, Yongzhan; Liang, Jie; Fan, Daiming

doi:10.1002/2211-5463.12363

Cited by 41 publications

(36 citation statements)

References 32 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miR-204 was previously reported to be involved in a series of physiological and pathological processes, such as diabetic retinopathy, aortic valve disease and ulcerative disease [25][26][27]. Some recent studies revealed that miR-204-5p also exerts antitumor effects on various cancers (e.g., breast cancer, melanoma and liver cancer) through inhibiting invasion and metastasis of cancer cells [25,[28][29][30]. This study found that miR-204-5p suppressed cell viability and invasion, and regulated the expressions of E-cadherin, N-cadherin and Twist1; moreover, LOC285758 could reduce the transcription of miR-204-5p and promoted AML cell viability and invasion.…”

Section: Discussionmentioning

confidence: 99%

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

Xue

Che

2020

FEBS Open Bio

View full text Add to dashboard Cite

Acute myeloid leukemia (AML) is the second most common type of leukemia worldwide. It was previously reported that expression of the long noncoding RNA LOC285758 is positively associated with AML cell proliferation, but the underlying mechanisms have not previously been reported. Here, we report that LOC285758 expression is higher in clinical AML blood samples and cultured AML cells. miR‐204‐5p was confirmed to be a target gene of LOC285758 by bioinformatics analysis and luciferase assay. LOC285758 overexpression promoted AML cell viability and invasion abilities, which were effectively inhibited by miR‐204‐5p overexpression; moreover, miR‐204‐5p overexpression also regulated the expression of E‐cadherin, N‐cadherin and Twist1. The data also showed that increased LOC285758 expression could effectively suppress the earlier effects of miR‐204‐5p on AML cells. Our findings suggest that targeting of miR‐204‐5p by LOC285758 promotes the cell viability and invasion of AML cells, and thus LOC285758 may have potential as a therapeutic target for AML treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

Xue

Che

2020

FEBS Open Bio

View full text Add to dashboard Cite

show abstract

“…In addition, we found that other microRNAs were involved in the regulation of tumor growth, proliferation, and apoptosis. For example, miR‐204‐5p inhibited the proliferation of hepatocellular carcinoma by directly regulating SIX1 and its downstream factors (Chu et al, ). MiR‐500a‐5p was identified as an oxidative stress miRNA whose activity may define breast cancer progression and survival (Degli Esposti et al, ).…”

Section: Discussionmentioning

confidence: 99%

Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis

Liu

Zhuang

et al. 2019

Molec Gen & Gen Med

View full text Add to dashboard Cite

Background Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasm that arises from the acquisition of constitutively active BCR‐ABL tyrosine kinase in hematopoietic stem cells. The persistence of bone marrow leukemia stem cells (LSCs) is the main cause of TKI resistance and CML relapse. Therefore, finding a key target or pathway to selectively target LSCs is of great significance for the thorough treatment of CML. Methods In this study, we aimed to identify key microRNAs, microRNA targets and pathways for the treatment of CML LSCs by integrating analyses of three microarray data profiles. We identified 51 differentially expressed microRNAs through integrated analysis of GSE90773 and performed functional gene predictions for microRNAs. Then, GSE11889 and GSE11675 were integrated to obtain differentially expressed genes (DEGs), and the overlapping DEGs were used as models to identify predictive functional genes. Finally, we identified 116 predictive functional genes. Clustering and significant enrichment analysis of 116 genes was based on function and signaling pathways. Subsequently, a protein interaction network was constructed, and module analysis and topology analysis were performed on the network. Results A total of 11 key candidate targets and 33 corresponding microRNAs were identified. The key pathways were mainly concentrated on the PI3K/AKT, Ras, JAK/STAT, FoxO and Notch signaling pathways. We also found that LSCs negatively regulated endogenous and exogenous apoptotic pathways to escape from apoptosis. Conclusion We identified key candidate targets and pathways for CML LSCs through bioinformatics methods, which improves our understanding of the molecular mechanisms of CML LSCs. These candidate genes and pathways may be therapeutic targets for CML LSCs.

show abstract

“…Although asthma is commonly diagnosed in childhood, it occurs in all age groups [3]. Ra et al reported that there was no significant difference between the prevalence rate of the elderly (>65) and that of the young people (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34) [4]. A lot of stimuli, including cold air and exercise, and other risk factors such as smoking, obesity and rhinitis contribute to asthma incidence [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

MiR-203a-3p regulates TGF-β1-induced epithelial–mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1

Fan

2020

Bioscience Reports

View full text Add to dashboard Cite

Asthma is a common chronic airway disease with increasing prevalence. MicroRNAs act as vital regulators in cell progressions and have been identified to play crucial roles in asthma. The objective of the present study is to clarify the molecular mechanism of miR-203a-3p in the development of asthma. The expression of miR-203a-3p and Sine oculis homeobox homolog 1 (SIX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of SIX1, fibronectin, E-cadherin, vimentin, phosphorylated-drosophila mothers against decapentaplegic 3 (p-Smad3) and Smad3 were measured by Western blot. The interaction between miR-203a-3p and SIX1 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. MiR-203a-3p was down-regulated and SIX1 was up-regulated in asthma serums, respectively. Transforming growth factor-β1 (TGF-β1) treatment induced the reduction of miR-203a-3p and the enhancement of SIX1 in BEAS-2B and 16HBE cells in a time-dependent manner. Subsequently, functional experiments showed the promotion of epithelial–mesenchymal transition (EMT) induced by TGF-β1 treatment could be reversed by miR-203a-3p re-expression or SIX1 deletion in BEAS-2B and 16HBE cells. SIX1 was identified as a target of miR-203a-3p and negatively regulated by miR-203a-3p. Then rescue assay indicated that overexpressed miR-203a-3p ameliorated TGF-β1 induced EMT by regulating SIX1 in BEAS-2B and 16HBE cells. Moreover, miR-203a-3p/SIX1 axis regulated TGF-β1 mediated EMT process in bronchial epithelial cells through phosphorylating Smad3. These results demonstrated that MiR-203a-3p modulated TGF-β1-induced EMT in asthma by regulating Smad3 pathway through targeting SIX1.

show abstract

miR‐204‐5p suppresses hepatocellular cancer proliferation by regulating homeoprotein SIX1 expression

Cited by 41 publications

References 32 publications

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

The long non‐coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down‐regulating miR‐204‐5p

Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis

MiR-203a-3p regulates TGF-β1-induced epithelial–mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1

Contact Info

Product

Resources

About