miR-145-5p Suppresses Breast Cancer Progression by Inhibiting SOX2

Tang, Wei; Zhang, Xiaoshen; Tan, Weige; Gao, Jin; Pan, Langxing; Ye, Xigang; Chen, Lun; Zheng, Wenbo

doi:10.1016/j.jss.2018.11.030

Cited by 63 publications

(45 citation statements)

References 20 publications

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“…Similarly, miR-145 expression has been associated with improved patient survival in other cancers, including esophageal squamous cell carcinoma and cervical cancer, suggesting a wider tumor suppressor role for miR-145 [25,26]. Ectopic expression of miR-145 decreased breast cancer cell proliferation and increased apoptosis in colorectal cancer cell lines [27,28]. Similarly, we observed a significant increase in apoptosis in our neuroblastoma cell lines following over-expression of miR-145 in vitro.…”

Section: Discussionsupporting

confidence: 72%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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Neuroblastoma (NB) is responsible for 15% of all childhood cancer deaths. Despite advances in treatment and disease management, the overall 5-year survival rates remain poor in high-risk disease (25-40%). It is well known that miR-145 functions as a tumor suppressor in several types of cancer. However, the impact of miR-145 on NB is still ambiguous. Our aim was to investigate the potential tumor suppressive role and mechanisms of miR-145 in high-risk neuroblastoma. Expression levels of miR-145 in tissues and cells were determined using RT-qPCR. The effect of miR-145 on cell viability was evaluated using MTT assays, apoptosis levels were determined using TUNEL staining, and the MTDH protein expression was determined using western blot and RT-PCR. Luciferase reporter plasmids were constructed to confirm direct targeting for MTDH. The results showed that miR-145 expression was significantly lower in high-risk MYCN amplified (MNA) tumors and low miR-145 expression was associated with worse EFS and OS in our cohort. Over-expression of miR-145 reduced cell viability and increased apoptosis in SH-SY-5Y cells. We identified MTDH as a direct target for miR-145 in SH-SY-5Y cells. Targeting MTDH has the similar results as miR-145 overexpression. Our findings suggest that low miR-145 expression was associated with poor prognosis in patients with NB, and the overexpression of miR-145 inhibited NB cells growth by down-regulating MTDH, thus providing a potential target for the development of microRNA-based approach for NB therapy.

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Section: Discussionsupporting

confidence: 72%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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“…In addition, miR-145 has been confirmed to have the potential serving as a candidate biomarker for human diagnosis. 15 Sathyanarayanan et al also found that miR-145 inhibited the proliferation and metastasis of CC cells by targeting SIP1. 16 Moreover, some bioinformatics studies have reported that the down-regulation of miR-145 is associated with poor prognosis of CC.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Cao¹,

Pan²,

Tang³

et al. 2020

OTT

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Objective: Cervical carcinoma (CC) is a serious threat to women's health and few effective therapeutic methods have been discovered. The purpose of this study is to explore the underlying mechanism of miR-145-5p in CC. Methods: Bioinformatics methods were employed to analyze the gene expression data of CC from TCGA database. qRT-PCR was used to detect the expression of miR-145-5p and KLF5 in CC cells, and Western blot was employed for the examination of KLF5 protein level. The targeted relationship between miR-145-5p and KLF5 was verified by a dualluciferase reporter assay. Moreover, CCK-8, wound healing assay and transwell invasion assay were used to analyze the effects of miR-145-5p overexpression or KLF5 silencing on the proliferation, migration and invasion of CC cells. Results: miR-145-5p was shown to be down-regulated in CC tissues and cells, while KLF5 was up-regulated. miR-145-5p could bind to the complementary sequence within the wild type KLF5 3ʹUTR rather than the mutant one. In addition, miR-145-5p could effectively down-regulate KLF5, in turn inhibiting the proliferation, migration and invasion of CC cells. Conclusion: miR-145-5p regulates the proliferation, migration and invasion of CC cells by targeting KLF5.

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“…In the present study, miRNA expression profiles were analyzed in a series of hereditary breast tumors (BRCA1/2 and BRCAX-associated breast tumors), sporadic breast tumors and NBT from BRCA1/2-germline mutation carriers and non-carriers using NanoString nCounter Technology. Initially, we identified differentially expressed miRNAs that could determine a specific signature of SBC vs. NBT that are related to miRNAs identified in previous studies about sporadic breast tumors (i.e., hsa-miR-145-5p, hsa-miR-429, hsa-miR-137, and hsa-miR-551a) [43][44][45][46]. Furthermore, this analysis was important to identify a specific miRNA signature for SBC and to investigate if any miR-NAs are shared between SBC and HBC.…”

Section: Discussionmentioning

confidence: 99%

miRNA expression profiling of hereditary breast tumors from BRCA1- and BRCA2-germline mutation carriers in Brazil

et al. 2020

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Background: MicroRNAs (miRNAs) are small non-coding RNAs involved in post-transcriptional gene expression regulation and have been described as key regulators of carcinogenesis. Aberrant miRNA expression has been frequently reported in sporadic breast cancers, but few studies have focused on profiling hereditary breast cancers. In this study, we aimed to identify specific miRNA signatures in hereditary breast tumors and to compare with sporadic breast cancer and normal breast tissues. Methods: Global miRNA expression profiling using NanoString technology was performed on 43 hereditary breast tumors (15 BRCA1, 14 BRCA2, and 14 BRCAX), 23 sporadic breast tumors and 8 normal breast tissues. These normal breast tissues derived from BRCA1and BRCA2mutation carriers (n = 5) and non-mutation carriers (n = 3). Subsequently, we performed receiver operating characteristic (ROC) curve analyses to evaluate the diagnostic performance of differentially expressed miRNAs. Putative target genes of each miRNAs considered as potential biomarkers were identified using miRDIP platform and used for pathway enrichment analysis. Results: miRNA expression analyses identified several profiles that were specific to hereditary breast cancers. A total of 25 miRNAs were found to be differentially expressed (fold change: > 2.0 and p < 0.05) and considered as potential biomarkers (area under the curve > 0.75) in hereditary breast tumors compared to normal breast tissues, with an expressive upregulation among BRCAX cases. Furthermore, bioinformatic analysis revealed that these miRNAs shared target genes involved in ErbB, FoxO, and PI3K-Akt signaling pathways. Conclusions: Our results showed that miRNA expression profiling can differentiate hereditary from sporadic breast tumors and normal breast tissues. These miRNAs were remarkably deregulated in BRCAX hereditary breast cancers. Therefore, miRNA signatures can be used as potential novel diagnostic biomarkers for the prediction of BRCA1/2germline mutations and may be useful for future clinical management.

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miR-145-5p Suppresses Breast Cancer Progression by Inhibiting SOX2

Cited by 63 publications

References 20 publications

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

miRNA expression profiling of hereditary breast tumors from BRCA1- and BRCA2-germline mutation carriers in Brazil

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