miR-125a-5p expression is associated with the age of breast cancer patients

He, Hua; Xu, Fang; Huang, Wei; Luo, Shuang; Lin, Yu; Zhang, G H; Du, Qiaoling; Duan, Ranhui

doi:10.4238/2015.december.22.17

Cited by 18 publications

(11 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miRNA-125 (miR-125) is a highly conserved miRNA family identified in diverse species from nematodes to humans. miR-125 family members are downregulated in several diseases, such as various cancers [ 12 , 13 ]. However, miR-125-5p is highly expressed in mature glial cells but is downregulated in retinal neurons [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

et al. 2018

View full text Add to dashboard Cite

BackgroundA deficiency of maternal thyroid hormones (THs) during pregnancy has severe impacts on fetal brain development. Neural stem cells (NSCs) are major targets of THs and provided a powerful model to explore the underlying mechanism of THs during brain development. Although miRNA-125 might be associated with the NSCs differentiation, the relationship between miR-125 and hypothyroidism (HypoT) development remains unclear.Material/MethodsIn our study, we screened a differentially expressed gene miR-125b-5p from brain between euthyroid (EuT) and HypoT rats. In vitro, we employed anion exchange resin to remove THs to stimulate HypoT. QRT-PCR and Western blot were used to examine the expression of signal transducer and activator of transcription 3 (Stat3). The relationship between miR-125b-5p and Stat3 was detected via a dual-luciferase assay.ResultsQRT-PCR results showed that the level of miR-125b-5p in HypoT rat brains was significantly suppressed, suggesting some relationship between miR-125b-5p and HypoT. In C17.2, miR-125b-5p promoted cell differentiation into neurons by regulating the expression of tubulin beta chain 3 (TUBB3) and glial fibrillary acid protein (GFAP). QRT-PCR and Western blot results revealed that miR-125b-5p mimic modulated the contents of total Stat3 and p-Stat3. A dual-luciferase assay showed that miR-125b-5p negatively regulated the expression of Stat3 by binding with the first site in 3′ UTR of Stat3.ConclusionsThese results revealed Stat3 is a new target of miR-125b-5p and revealed the mechanism of miR-125b-5p suppressing HypoT development. These findings provide a new target for HypoT therapy.

show abstract

Section: Introductionmentioning

confidence: 99%

miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

et al. 2018

View full text Add to dashboard Cite

show abstract

“…In addition, BDNF serves as a vital regulator of energy balance . Xu et al reported that miR‐125a‐5p served as a tumour suppressor by regulating the BRCA1 signalling in breast cancer cells, whereas He et al demonstrated that miR‐125a‐5p may play an important role in breast cancer progression in an age‐dependent manner . miR148a as one of the hypermethylated miRNAs exhibiting cancer‐specific methylation epigenetic is specifically and preferentially expressed in mouse epididymis .…”

Section: Discussionmentioning

confidence: 99%

Differential expression of microRNAs in TM3 Leydig cells of mice treated with brain‐derived neurotrophic factor

Gao

et al. 2017

Cell Biochemistry & Function

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that can promote the development and proliferation of neurons. BDNF has been found to be involved in male reproduction. Leydig cells in testicular interstitial tissues can secrete testosterone in a luteinizing hormone-dependent manner. We showed that BDNF and its receptor TrkB were expressed in mice TM3 Leydig cells in the present study. Furthermore, BDNF can promote proliferation of mouse TM3 Leydig cells in vitro. Results of microRNA (miRNA) deep sequencing showed that BDNF can alter the expression profile of miRNAs in TM3 Leydig cells. Eighty-three miRNAs were significantly different in the BDNF-treated and control groups (fold change of >2.0 or <0.5, P < 0.05) wherein 40 were upregulated and 43 were downregulated. The expression levels of miR-125a-5p, miR-22-5p, miR-342-59, miR-451a, miR-148a-5p, miR-29b-3p, miR-199b-5p, and miR-145a-5p were further confirmed by quantitative real-time polymerase chain reaction. Bioinformatic analysis revealed that miRNAs regulated a large number of genes with different functions. Pathway analysis indicated that miRNAs participate in the pathways involved in signal transduction, cancer, metabolism, endocrine system, immune system, and nerve system. This study indicated that miRNAs might be involved in the BDNF-regulated cellular functions of Leydig cells.

show abstract

“…Finally, miR-192 was found to directly target SCARB1 mRNA in adipocytes (Mysore et al, 2016 ). Although no data on the role of these miRNAs in the context of SCARB1 and cancer is available, recent studies have shown that levels of miR-125a (Guo et al, 2009 ; He et al, 2015 ; Tong et al, 2015 ; Lee et al, 2016 ), miR-455 (Chai et al, 2015 ; Li et al, 2016 ), miR-185 (Qu et al, 2013 ; Fu et al, 2014 ; Tang et al, 2014 ; Li et al, 2015 ; Zhang et al, 2015 ), and miR-192 (Feng et al, 2011 ; Geng et al, 2014 ; Sun et al, 2016 ) are down-regulated in several types of cancer. These findings suggest that SCARB1 post-transcriptional regulation may be altered to promote SR-BI expression in cancer cells.…”

Section: Regulations Of Scarb1 Transcription and Smentioning

confidence: 99%

SR-BI: Linking Cholesterol and Lipoprotein Metabolism with Breast and Prostate Cancer

et al. 2016

View full text Add to dashboard Cite

Studies have demonstrated the significant role of cholesterol and lipoprotein metabolism in the progression of cancer. The SCARB1 gene encodes the scavenger receptor class B type I (SR-BI), which is an 82-kDa glycoprotein with two transmembrane domains separated by a large extracellular loop. SR-BI plays an important role in the regulation of cholesterol exchange between cells and high-density lipoproteins. Accordingly, hepatic SR-BI has been shown to play an essential role in the regulation of the reverse cholesterol transport pathway, which promotes the removal and excretion of excess body cholesterol. In the context of atherosclerosis, SR-BI has been implicated in the regulation of intracellular signaling, lipid accumulation, foam cell formation, and cellular apoptosis. Furthermore, since lipid metabolism is a relevant target for cancer treatment, recent studies have focused on examining the role of SR-BI in this pathology. While signaling pathways have initially been explored in non-tumoral cells, studies with cancer cells have now demonstrated SR-BI's function in tumor progression. In this review, we will discuss the role of SR-BI during tumor development and malignant progression. In addition, we will provide insights into the transcriptional and post-transcriptional regulation of the SCARB1 gene. Overall, studying the role of SR-BI in tumor development and progression should allow us to gain useful information for the development of new therapeutic strategies.

show abstract

miR-125a-5p expression is associated with the age of breast cancer patients

Cited by 18 publications

References 20 publications

miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

miRNA-125b-5p Suppresses Hypothyroidism Development by Targeting Signal Transducer and Activator of Transcription 3

Differential expression of microRNAs in TM3 Leydig cells of mice treated with brain‐derived neurotrophic factor

SR-BI: Linking Cholesterol and Lipoprotein Metabolism with Breast and Prostate Cancer

Contact Info

Product

Resources

About