miR‑199b‑5p inhibits triple negative breast cancer cell proliferation, migration and invasion by targeting DDR1

Wu, Anhao; Chen, Yan; Liu, Yang; Lai, Yafang; Liu, Dequan

doi:10.3892/ol.2018.9255

Cited by 25 publications

(23 citation statements)

References 26 publications

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“…In triple negative breast cancer (TNBC) cells, miR-199b suppresses cell proliferation and invasion by directly targeting DDR1. 38 BC patients who showed lower expression level of miR-199b had poorer overall survival rate than those with high level. Furthermore, it is indicated that low expression of miR-199b is correlated with poor prognosis, advanced TNM stage, and positive lymph node metastasis in BC.…”

Section: Discussionmentioning

confidence: 91%

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Aberrant expression of a five‐microRNA signature in breast carcinoma as a promising biomarker for diagnosis

Bitaraf

Babashah

Garshasbi

2019

Clinical Laboratory Analysis

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Background Breast cancer (BC) is the most common malignancy among females with dismal quality of life in patients. It has been proven that epigenetic factors, especially microRNAs, are involved in breast carcinogenesis and progression. This study aimed to assess the expression and clinical performances of a five‐microRNA signature (miR‐127‐3p, miR‐133a‐3p, miR‐155‐5p, miR‐199b‐5p, and miR‐342‐5p) in breast cancer and adjacent normal tissues to identify a potential biomarker for BC and investigate the relationship between their expression and clinicopathological features of BC patients as well. Methods In this case‐control investigation, we recruited 50 pairs of tumor and matched non‐tumor surgical specimens from patients diagnosed with BC. Expression levels of miR‐127‐3p, miR‐133a‐3p, miR‐155‐5p, miR‐199b‐5p, and miR‐342‐5p were measured in BC and adjacent normal tissues by RT‐qPCR. Results We found that miR‐127‐3p, miR‐133a‐3p, miR‐199b‐5p, and miR‐342‐5p were significantly down‐regulated, while miR‐155‐5p was significantly up‐regulated in BC tumor tissues compared with the corresponding adjacent normal tissues. The decreased expression of miR‐127‐3p, miR‐133a‐3p, miR‐342‐5p, and up‐regulation of miR‐155‐5p showed a significant correlation with disease stage. We also found a significant down‐regulation of miR‐127‐3p, miR‐199b‐5p, and miR‐342‐5p compared in HER‐2‐negative patients. Our results indicated that miR‐155‐5p had a higher expression level in HER‐2‐positive patients. Receiver operating characteristic (ROC) curve analysis demonstrated that all these five microRNAs can serve as potential biomarkers to distinguish between tumor and non‐tumor breast tissue samples. Conclusions The present findings suggested that dysregulation of this five‐miRNA signature might be considered as a promising and functional biomarker for BC diagnosis.

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Section: Discussionmentioning

confidence: 91%

“…It has been shown that miR‐199b acts as a tumor suppressor in BC. In triple negative breast cancer (TNBC) cells, miR‐199b suppresses cell proliferation and invasion by directly targeting DDR1 . BC patients who showed lower expression level of miR‐199b had poorer overall survival rate than those with high level.…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of a five‐microRNA signature in breast carcinoma as a promising biomarker for diagnosis

Bitaraf

Babashah

Garshasbi

2019

Clinical Laboratory Analysis

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“…However, emerging studies have confirmed that different miRNAs play diverse roles in TNBC, some as tumorigenic agents, and some as tumor inhibitors. For example, as tumorigenic agents, miR-25, 16 miR-20, 17 miR-224, 18 miR-135 19 and miR-301 20 promote the occurrence and development of TNBC, whereas miR-124, 15 miR-4417, 21 miR-4306, 22 miR-199, 23 miR-1287 24 and miR-3178 25 as tumor inhibitors inhibit the oncogenesis and development of TNBC. In this study, relative miR-153 expression in TNBC tissues and cells was remarkably lower than that in corresponding adjacent noncancerous tissues and normal breast epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Shi

Fan

et al. 2019

OTT

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Background: Triple-negative breast cancer (TNBC) is the most malignant type of breast cancer. MicroRNAs (miRs) and their corresponding molecular targets are associated with the occurrence and development of various human malignancies. However, the roles of the microRNA-153 (miR-153) and zinc finger E-box-binding homeobox 2 (ZEB2)-induced epithelial-mesenchymal transition (EMT) in TNBC and predictive effect of miR-153 on the prognosis of TNBC have not been fully elucidated. Materials and methods: Relative miR-153 expression level was examined by RT-qPCR assay in TNBC tissues of 60 patients and TNBC cell lines (SKBR3, BT-549 and MDA-MB-231). Cell proliferation ability, invasion ability and migration ability were measured by CCK8 assay, Transwell invasion assay and wound healing assay, respectively. Luciferase reporting experiment was used to confirm that there was a miR-153-binding site in ZEB2 3ʹ-UTR. The expression of ZEB2 in tissues and its relationship with miR-153 were analyzed with immunohistochemistry method. Relative ZEB2, E-cadherin, N-cadherin and Vimentin mRNA and protein expression levels were observed with RT-qPCR and Western blot, respectively. Based on risk factors, a prognostic model was established according to the Cox proportional risk model, and the prognostic risk factors of TNBC patients were predicted and analyzed. Results: The expression of miR-153 in TNBC tissues and cells was declined (all P<0.01), and upregulation of miR-153 inhibited proliferation, invasion and migration of TNBC cells (all P<0.01). In addition, miR-153 regulated ZEB2/EMT link in TNBC, and ZEB2 overexpression reversed the tumor-suppressive effect of miR-153 in TNBC. Moreover, miR-153 was an independent predictive factor that was associated with excellent prognosis in TNBC patients. Conclusion: miR-153 may inhibit TNBC proliferation, invasion and migration by regulating ZEB2/EMT link. Therefore, miR-153 is expected to be a molecular target and prognostic marker for TNBC.

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“…Previous studies documented that DDR1 expression can be regulated at the transcription level by factors such as tumor protein p53 (TP53) and zinc finger E-box binding homeobox 1 (13) or promoter CpG methylation (49). DDR1 expression may be also controlled post-transcriptionally by the two highly similar miRs, miR-199a-5p and miR-199b-5p as found in hepatocellular carcinoma (35), acute myeloid leukemia (42), colorectal cancer (37), cutaneous squamous cell carcinoma (39) or triple-negative breast cancer (54). The expression levels of miR-199a-5p or miR-199b-5p were negatively correlated with DDR1 protein content in the ccRCC tissues, suggesting that those two miRs may repress DDR1 in ccRCC.…”

Section: Discussionmentioning

confidence: 99%

Altered Expression of DDR1 in Clear Cell Renal Cell Carcinoma Correlates With miR-199a/b-5p and Patients' Outcome

Krazinski

Kiewisz

Sliwinska-Jewsiewicka

et al. 2019

Cancer Genomics Proteomics

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Background/Aim. Accumulating evidence suggests that discoidin domain receptor tyrosine kinase 1 (DDR1) has an oncogenic role. Therefore, the aim of this study was to evaluate the potential utility of DDR1 and its posttranscriptional repressors, miR-199a-5p and miR-199b-5p, as prognostic factors in clear cell renal cell carcinoma (ccRCC). Patients and Methods. The expression of DDR1 in tumor and normal renal tissues of 56 patients with ccRCC was assessed by reverse transcription quantitative polymerase chain reaction, western blotting and immunohistochemistry. Renal cancer cells were transfected with specific RNA sequences to validate DDR1 as a putative miR-199a/b-5p target. Results. Decreased DDR1 mRNA and protein, as well as miR-199a/b-5p levels were found in ccRCC. Low DDR1 protein was associated with higher nuclear grade and shorter overall survival. DDR1 immunoreactivity was elevated in the nuclei and unchanged in the membrane/cytoplasmic compartment of tumor cells. DDR1 levels correlated with those of miR-199a/b-5p. In addition, we validated DDR1 as a target gene for miR-199a/b-5p in renal cancer cell lines. Conclusion. DDR1 expression is altered in ccRCC, but our findings do not support its oncogenic role. Indepth investigation will be necessary to elucidate the exact role and potential utility of miR-199a/b-5p in ccRCC. Renal cell carcinoma (RCC) is considered one of the most lethal urological malignancies representing the sixth and tenth most frequently diagnosed cancers in men and women, respectively (1). The most prevalent histological subtype of RCC, clear cell renal cell carcinoma (ccRCC) comprises 70-80% of renal tumors (2). It is believed that clear cell tumors originate in the proximal convoluted tubule (PCT) (3, 4). The majority of ccRCC sporadic cases are characteristically associated with the loss of function of von Hippel-Lindau (VHL) tumor-suppressor gene by somatic mutations, chromosomal loss or promoter hypermethylation (5). Loss or inactivation of VHL results in a sequence of events comprising accumulation of hypoxia inducible factors (HIFs), overexpression of HIF-driven genes such as vascular endothelial growth factor (VEGF), promotion of angiogenesis, cell proliferation and tumor growth (5). Surgical resection is the mainstay of treatment of localized renal tumors, although a significant number of these patients will eventually develop recurrent or metastatic disease (2). Better understanding of ccRCC molecular background allowed for introduction of new therapeutics that target VEGF and mammalian target of rapamycin (mTOR) pathways and can be applied in the adjuvant pharmacotherapy of advanced or metastatic tumors. However, the benefits of ccRCC adjuvant therapies are still far below expectations and complete and durable responses are rare (4). At present, RCC recurrence risk stratification models are primarily based on the American Joint Committee on Cancer (AJCC) pathological tumor-node-metastasis (TNM) classification and histopathological features (2, 4, 6). To date, 179 This article i...

show abstract

miR‑199b‑5p inhibits triple negative breast cancer cell proliferation, migration and invasion by targeting DDR1

Cited by 25 publications

References 26 publications

Aberrant expression of a five‐microRNA signature in breast carcinoma as a promising biomarker for diagnosis

Aberrant expression of a five‐microRNA signature in breast carcinoma as a promising biomarker for diagnosis

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Altered Expression of DDR1 in Clear Cell Renal Cell Carcinoma Correlates With miR-199a/b-5p and Patients' Outcome

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