MicroRNA-223-3p inhibits human bladder cancer cell migration and invasion

Guo, Ju; Cao, Runfu; Yu, Xingwei; Xiao, Zewen; Chen, Zhiwen

doi:10.1177/1010428317691678

Cited by 17 publications

(16 citation statements)

References 21 publications

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“…Usually, miR-223 was considered to be a suppressor in multiple cancers, such as cervical cancer [28], bladder cancer [29], prostate cancer [30] and breast cancer [31]. Our results were consistent with these previous findings.…”

Section: Discussionsupporting

confidence: 83%

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

Yang¹,

Jiang

Ma³

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the cellular effects and clinical significance of microRNA-223 (miR-223) in breast cancer by targeting stromal interaction molecule1 (STIM1). Methods: Breast cancer cell lines (T47D, MCF-7, SKB-R3, MDA-MB-231 and MDA-MB-435) and a normal breast epithelial cell line (MCF-10A) were prepared for this study. MiR-223 mimics, anti-miR-223 and pcDNA 3.1-STIM1 were transiently transfected into cancer cells independently or together, and then RT-qPCR was performed to detect the expressions of miR-223 and STIM1 mRNA, dual-luciferase reporter assay was conducted to examine the effects of miR-223 on STIM1, Western blotting was used to measure the expressions of the STIM1 proteins, MTT and Trans-well assays were performed to detect cell proliferation and invasion. Finally, the correlation of miR-223 and STIM1 was investigated by detecting with ISH and IHC in breast cancer specimens or the corresponding adjacent normal tissues. Results: Compared with normal cells and tissues, breast cancer tissues and cells exhibited significantly lower expression of miR-223, but higher expression of STIM1. MiR-223 could inhibit the proliferation and invasiveness of breast cancer cells by negatively regulating the expressions of STIM1. Reimplantation with STIM1 partially rescued the miRNA-223-induced inhibition of breast cancer cells. Clinical data revealed that high expression of STIM1 and miR-223 was respectively detrimental and beneficial factor impacting patient’s disease-free survival (DFS) rather than overall survival (OS). Moreover, Pearson correlation analysis also confirmed that STIM1 was inversely correlated with miR-223. Conclusion: MiR-223 inhibits the proliferation and invasion of breast cancer by targeting STIM1. The miR-223/STIM1 axis could possibly be a potential therapeutic target for treating breast cancer patients.

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Section: Discussionsupporting

confidence: 83%

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

Yang¹,

Jiang

Ma³

et al. 2018

Cell Physiol Biochem

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“…miRNAs are also involved in modulating different cancer-related biological processes, such as cell proliferation, cycle, apoptosis, angiogenesis, invasion, migration and metastasis (12)(13)(14). Moreover, numerous miRNAs are aberrantly expressed in various kinds of human cancers, such as EOC (15), cervical cancer (16), gastric cancer (17), lung cancer (18) and bladder cancer (19). miRNAs may act as either oncogenes or tumor suppressors in tumor initiation and progression on the basis of the biological roles of their target genes (20).…”

Section: Microrna-455 Inhibits Cell Proliferation and Invasion Of Epimentioning

confidence: 99%

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

et al. 2017

Molecular Medicine Reports

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Ovarian cancer (OC) is the fifth leading cause of cancer‑associated mortality among women in developed countries. Numerous microRNAs are aberrantly expressed in epithelial (E) OC, and are involved in EOC formation and progression. As such, microRNAs may be investigated as diagnostic and prognostic molecular biomarkers, and therapeutic targets for patients with EOC. For instance, microRNA‑455 (miR‑455) is abnormally expressed in various types of human cancer. However, details on the expression level, biological roles and underlying mechanism of miR‑455 in EOC remain unclear. In the present study, the expression of miR‑455 in EOC was detected, and its association with clinical characteristics was analysed. The functional roles and underlying mechanisms of miR‑455 in EOC were also investigated. The results revealed that miR‑455 expression in EOC tissues and cell lines was significantly downregulated. Furthermore, miR‑455 downregulation was correlated with tumor size, International Federation of Gynecology and Obstetrics stage and lymph node metastasis of patients with EOC. Restoration of miR‑455 expression efficiently inhibited cell proliferation and invasion in vitro. Notch1 was identified as a direct target of miR‑455 in EOC. The mRNA and protein expression levels of Notch1 were higher in EOC tissues compared with in normal ovarian epithelial tissues. Spearman's correlation analysis indicated that miR‑455 expression was negatively correlated with the mRNA level of Notch1 in EOC tissues. Notch1 overexpression was able to restore the EOC cell proliferation and invasion abilities suppressed by miR‑455. The present study provided evidence that the dysregulation of the miR‑455/Notch1 signalling pathway may be essential for EOC occurrence and development. In addition, the results confirmed the tumor‑suppressive roles of miR‑455 in modulating EOC proliferation and invasion through regulation of Notch1 expression. Thus, miR‑455 may be a novel miRNA‑based therapeutic target to treat patients with EOC.

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“…Besides genetic variations, post-transcriptional regulations also affected the functioning of associated enzymes. For instance, NCOA1 was confirmed as a target of miR-223-3p and demonstrated to have low expression levels (53,54). Evidence has indicated that changes to the microenvironment resulting from hypoxia, which is insufficient to maintain cellular function, were associated with cancer pathology.…”

Section: Univariate Analysis Multivariate Analysis ------------------mentioning

confidence: 99%

Comprehensive analysis of histone modification‑associated genes on differential gene expression and prognosis in gastric cancer

et al. 2019

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Accumulating evidence suggests that the epigenetic alterations caused by histone modifications have important roles in the genesis of gastric cancer (GC), particularly the well-studied acetylation and methylation modifications. In the present study, a Bioinformatics analysis of the expression of histone modification-associated genes in GC and normal tissues was performed by using datasets from Oncomine, the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). The clinical data of GC patients were downloaded from TCGA to determine the association between histone modification-associated gene expression and clinicopathological parameters or survival of GC. Finally, lysine acetyltransferase 2A (KAT2A), nuclear receptor coactivator 1 (NCOA1), SMYD family member 5 (SMYD5), protein arginine methyltransferase 1 (PRMT1) and PRDF1-RIZ (PR)/Su(var)3-9, enhancer-of-zeste and trithorax (SET) domain 16 (PRDM16) were screened; KAT2A, SMYD5 and PRMT1 were upregulated, while PRDM16 expression was downregulated in GC. Analysis of the GEO and Oncomine datasets revealed that NCOA1 was upregulated, which was contrary to the result obtained with the TCGA stomach adenocarcinoma dataset. Aberrant expression of KAT2A, NCOA1, SMYD5 and PRMT1 was more obvious in gastric intestinal-type adenocarcinoma; low NCOA1 expression was associated with better overall survival of GC patients [hazard ratio (HR)=0.690, 95% CI=0.570-0.840, P<0.001] and was an independent predictor for patients diagnosed with GC (HR=0.639, 95% CI=0.437-0.933, P=0.020). Correlation analysis and protein-protein interaction network analysis indicated a close association between ATAD2 and estrogen receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A. In conclusion, differential expression of KAT2A, NCOA1, SMYD5, PRMT1 and PRDM16 was identified in GC vs. normal tissues, low NCOA1 expression was associated with poor survival of GC and ATAD2 may interact with ESR1 to regulate NCOA1 and PRMT1 in GC.

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MicroRNA-223-3p inhibits human bladder cancer cell migration and invasion

Cited by 17 publications

References 21 publications

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

Comprehensive analysis of histone modification‑associated genes on differential gene expression and prognosis in gastric cancer

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