miR-151-3p Targets TWIST1 to Repress Migration of Human Breast Cancer Cells

Yeh, Ting Chih; Huang, Tzu Ting; Yeh, Tien Shun; Chen, Yu Ren; Hsu, Kai-Wen; Yin, Pen Hui; Tseng, Ling Ming

doi:10.1371/journal.pone.0168171

Cited by 39 publications

(22 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The evidence about miR-151-3p is even scarcer. Several studies have observed a relationship with cancer 25,26 . Its association with atherosclerosis has not been reported to date.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction

Horváth

Horváthová

Hájek

et al. 2020

Sci Rep

View full text Add to dashboard Cite

We sought to analyse plasma levels of peripheral blood microRNAs (miRs) as biomarkers of ST-segmentelevation myocardial infarction (STEMI) due to type-1 myocardial infarction as a model situation of vulnerable plaque (VP) rupture. Samples of 20 patients with STEMI were compared both with a group of patients without angina pectoris in whom coronary angiogram did not reveal coronary atherosclerotic disease (no coronary atherosclerosis-NCA) and a group of patients with stable angina pectoris and at least one significant coronary artery stenosis (stable coronary artery disease-SCAD). This study design allowed us to identify miRs deregulated in the setting of acute coronary artery occlusion due to VP rupture. Based on an initial large scale miR assay screening, we selected a total of 12 miRs (three study miRs and nine controls) that were tested in the study. Two of the study miRs (miR-331 and miR-151-3p) significantly distinguished STEMI patients from the control groups, while ROC analysis confirmed their suitability as biomarkers. Importantly, this was observed in patients presenting early with STEMI, even before the markers of myocardial necrosis (cardiac troponin I, miR-208 and miR-499) were elevated, which suggests that the origin of miR-331 and miR-151-3p might be in the VP. In conclusion, the study provides two novel biomarkers observed in STEMI, which may be associated with plaque rupture. Rupture of a vulnerable atherosclerotic plaque (VP), which leads to acute artery occlusion due to an overlying thrombosis, is a potentially devastating situation resulting in acute coronary syndromes (ACS), ischaemic stroke and other acute complications of atherosclerosis 1-5. Early detection of VP in vivo is essential for effective primary prevention of their rupture, which might aid in the reduction of cardiovascular morbidity and mortality 6. A potent biomarker that would be sensitive enough for the presence of a VP with a reasonable specificity could be a very important piece of this puzzle. MicroRNAs (miRs) are small, non-coding RNA molecules that act as modifiers of gene expression 7-9. Once they bind to their target mRNA, they may cause its degradation or suppression of its translation 7-9. Thus, miRs control many cellular processes and play a role in the pathogenesis of various diseases that include atherosclerosis 7-9. The molecules are very stable, easy to detect with quantitative polymerase chain reaction (qPCR) and are relatively tissue specific 9-12. Due to these properties, miRs appear to be very suitable biomarkers. The aim of this study was to identify plasma miRs from peripheral blood samples of patients with ST-segment-elevation myocardial infarction (STEMI) that might help quicken its diagnostics or may even be used directly as markers of VP. Such biomarkers might be used for the risk stratification of patients and both aid in tailoring the primary preventive measures and help as prognostic markers in patients with clinically manifested atherosclerosis.

show abstract

“…The evidence about miR-151-3p is even scarcer. Several studies have observed a relationship with cancer 25,26 . Its association with atherosclerosis has not been reported to date.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction

Horváth

Horváthová

Hájek

et al. 2020

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Evidences showed that Twist1 decreases the expression of E-cadhrin [ 19 , 27 , 28 , 29 ], and the lack of E-cadherin can induce the expression of Twist1, so forms a positive feedback, keep cells in an interstitial state, so as to induce the EMT. Like in breast cancer cells [ 9 ], in SiHa and CaSki cervical cancer cell lines, we also found by luciferase assay that Twist1 promoter activity and expression were decreased by TQ.…”

Section: Discussionmentioning

confidence: 99%

Thymoquinone Inhibits the Migration and Invasive Characteristics of Cervical Cancer Cells SiHa and CaSki In Vitro by Targeting Epithelial to Mesenchymal Transition Associated Transcription Factors Twist1 and Zeb1

Khan

Wei

et al. 2017

Molecules

View full text Add to dashboard Cite

Cervical cancer is one of the most common gynecological malignant tumors worldwide, for which chemotherapeutic strategies are limited due to their non-specific cytotoxicity and drug resistance. The natural product thymoquinone (TQ) has been reported to target a vast number of signaling pathways in carcinogenesis in different cancers, and hence is regarded as a promising anticancer molecule. Inhibition of epithelial to mesenchymal transition (EMT) regulators is an important approach in anticancer research. In this study, TQ was used to treat the cervical cancer cell lines SiHa and CaSki to investigate its effects on EMT-regulatory proteins and cancer metastasis. Our results showed that TQ has time-dependent and dose-dependent cytotoxic effects, and it also inhibits the migration and invasion processes in different cervical cancer cells. At the molecular level, TQ treatment inhibited the expression of Twist1, Zeb1 expression, and increased E-Cadherin expression. Luciferase reporter assay showed that TQ decreases the Twist1 and Zeb1 promoter activities respectively, indicating that Twist1 and Zeb1 might be the direct target of TQ. TQ also increased cellular apoptosis in some extent, but apoptotic genes/proteins we tested were not significant affected. We conclude that TQ inhibits the migration and invasion of cervical cancer cells, probably via Twist1/E-Cadherin/EMT or/and Zeb1/E-Cadherin/EMT, among other signaling pathways.

show abstract

“…Interestingly, BCL2L1 is regulated by miR-1266, miR-185, and miR-30c [60] in prostate cancer. TWIST1 is regulated by miR-151-3p in BC [61]. These miRNAs are involved in negative regulation of the apoptotic pathway and upregulation of invasion or migration respectively, but the role in BM is not clear yet.…”

Section: Extravasationmentioning

confidence: 99%

microRNAs Orchestrate Pathophysiology of Breast Cancer Brain Metastasis: Advances in Therapy

et al. 2020

View full text Add to dashboard Cite

Brain metastasis (BM) predominantly occurs in triple-negative (TN) and epidermal growth factor 2 (HER2)-positive breast cancer (BC) patients, and currently, there is an unmet need for the treatment of these patients. BM is a complex process that is regulated by the formation of a metastatic niche. A better understanding of the brain metastatic processes and the crosstalk between cancer cells and brain microenvironment is essential for designing a novel therapeutic approach. In this context, the aberrant expression of miRNA has been shown to be associated with BM. These non-coding RNAs/miRNAs regulate metastasis through modulating the formation of a metastatic niche and metabolic reprogramming via regulation of their target genes. However, the role of miRNA in breast cancer brain metastasis (BCBM) is poorly explored. Thus, identification and understanding of miRNAs in the pathobiology of BCBM may identify a novel candidate miRNA for the early diagnosis and prevention of this devastating process. In this review, we focus on understanding the role of candidate miRNAs in the regulation of BC brain metastatic processes as well as designing novel miRNA-based therapeutic strategies for BCBM.Keywords: Breast cancer brain metastasis, miRNA, Brain tumor microenvironment, Blood-brain barrier, CNS metastasis

show abstract

miR-151-3p Targets TWIST1 to Repress Migration of Human Breast Cancer Cells

Cited by 39 publications

References 42 publications

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction

Thymoquinone Inhibits the Migration and Invasive Characteristics of Cervical Cancer Cells SiHa and CaSki In Vitro by Targeting Epithelial to Mesenchymal Transition Associated Transcription Factors Twist1 and Zeb1

microRNAs Orchestrate Pathophysiology of Breast Cancer Brain Metastasis: Advances in Therapy

Contact Info

Product

Resources

About