miR-374a-5p promotes tumor progression by targeting ARRB1 in triple negative breast cancer

Sim

et al. 2019

J Pathol Transl Med

Background: Lung cancer is the most common cause of cancer-related death, and adenocarcinoma is the most common histologic subtype. MicroRNA is a small non-coding RNA that inhibits multiple target gene expression at the post-transcriptional level and is commonly dysregulated in malignant tumors. The purpose of this study was to analyze the expression of microRNA-374a (miR-374a) in lung adenocarcinoma and correlate its expression with various clinicopathological characteristics. Methods: The expression level of miR-374a was measured in 111 formalin-fixed paraffin-embedded lung adenocarcinoma tissues using reverse transcription-quantitative polymerase chain reaction assays. The correlation between miR-374a expression and clinicopathological parameters, including clinical outcome, was further analyzed. Results: High miR-374 expression was correlated with advanced pT category (chi-square test, p = .004) and pleural invasion (chi-square test, p = .034). Survival analysis revealed that patients with high miR-374a expression had significantly shorter disease-free survival relative to those with low miR-374a expression (log-rank test, p = .032). Conclusions: miR-374a expression may serve as a potential prognostic biomarker for predicting recurrence in early stage lung adenocarcinoma after curative surgery.

“…11 In triple-negative breast cancer, ARRB1 was a direct target of miR-374a, and knockdown of miR-374a attenuated cell proliferation and migration in vitro. 13 Long-rank test, p = .032…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA-374a Expression as a Prognostic Biomarker in Lung Adenocarcinoma

Sim

et al. 2019

J Pathol Transl Med

“…On the other hand, oncogenic miRNAs also play crucial roles in TNBC. MiR‐498, miR‐374a‐5p and miR‐761 were significantly overexpressed in TNBC and promoted cell proliferation and migration by downregulating PTEN, ARRB1 and TRIM29, respectively 37‐39 . Moreover, the miR‐106b‐25 cluster mediated oncogenesis in breast cancer by activation of NOTCH1 by targeting NEDD4L in both ER+ and TNBC breast cancer cells, suggesting that the miR‐106b‐25/NEDD4L/NOTCH1 axis played a crucial role in breast cancer 40 .…”

Section: Micrornasmentioning

confidence: 99%

Systematic characterization of non‐coding RNAs in triple‐negative breast cancer

et al. 2020

Triple‐negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer with negativity for oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor (HER2). Non‐coding RNAs (ncRNAs) make up most of the transcriptome and are widely present in eukaryotic cells. In recent years, emerging evidence suggests that ncRNAs, mainly microRNAs (miRNAs), long ncRNAs (lncRNAs) and circular RNAs (circRNAs), play prominent roles in the tumorigenesis and development of TNBC, but the functions of most ncRNAs have not been fully described. In this review, we systematically elucidate the general characteristics and biogenesis of miRNAs, lncRNAs and circRNAs, discuss the emerging functions of these ncRNAs in TNBC and present future perspectives in clinical practice.

Journal of Experimental Medicine

“…About 20% of BCs in China are TNBC subtype (Peng et al, 2016). TNBC is the most aggressive subtype of BC and is associated with worst prognosis and overall survival (OS; Son et al, 2019). It is characterized by high cell proliferation, poor cellular differentiation, and more frequent disease recurrence (Chang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

LncRNA-encoded polypeptide ASRPS inhibits triple-negative breast cancer angiogenesis

Wang

Zhu

et al. 2019

162

101

Triple-negative breast cancer (TNBC) is a subtype of breast cancer (BC) with the most aggressive phenotype and poor overall survival. Using bioinformatics tools, we identified LINC00908 encoding a 60–aa polypeptide and differentially expressed in TNBC tissues. We named this endogenously expressed polypeptide ASRPS (a small regulatory peptide of STAT3). ASRPS expression was down-regulated in TNBCs and associated with poor overall survival. We showed that LINC00908 was directly regulated by ERα, which was responsible for the differential down-regulation of LINC00908 in TNBCs. ASRPS directly bound to STAT3 through the coiled coil domain (CCD) and down-regulated STAT3 phosphorylation, which led to reduced expression of VEGF. In human endothelial cells, a mouse xenograft breast cancer model, and a mouse spontaneous BC model, ASRPS expression reduced angiogenesis. In a mouse xenograft breast cancer model, down-regulation of ASRPS promoted tumor growth, and ASRPS acted as an antitumor peptide. We presented strong evidence that LINC00908-encoded polypeptide ASRPS represented a TNBC-specific target for treatment.