MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Wang, Jingjie; Zeng, Huijuan; Li, Hanjun; Chen, Tao; Wang, Lulu; Zhang, Kai; Chen, Jing; Wang, Rui; Li, Qiurong; Wang, Shaohua

doi:10.1159/000481445

Cited by 44 publications

(36 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although neoadjuvant and systemic chemotherapy has been widely used to treat breast cancer, successful molecular-targeted therapies of any type are currently unavailable [5]. Recent studies have started to focus on the roles of miR in breast cancer development and progression [6, 7]. …”

Section: Introductionmentioning

confidence: 99%

MicroRNA-34a Inhibition of the TLR Signaling Pathway Via CXCL10 Suppresses Breast Cancer Cell Invasion and Migration

Xu¹,

Liu²,

Yang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Breast cancer (BC) starts as a local disease, but it can metastasize to the lymph nodes and distant organs. However, the metastatic process is still poorly understood. The mRNA microarray datasets GSE26910 and GSE33447 show that CXCL10 is up-regulated in BC, and the microRNA microarray dataset GSE38167 and a network meta-analysis of microRNA expression profile studies in human BC suggest that microRNA-34a (miR-34a) is down-regulated in BC. CXCL10 was predicted as a target of miR-34a by microRNA.org. In this study, we uncovered a CXCL10-independent mechanism by which miR-34a exerts its antimetastatic activity in BC. Methods: To investigate the clinical significance of miR-34a in BC, we collected cancer tissues and paracancerous tissues from 258 patients with BC. In addition, a series of inhibitors, mimics, and siRNAs was introduced into MCF-7 and T47D cells to validate the regulatory mechanisms by which miR-34a regulates CXCL10. Next, to better understand the pivotal role of TLR signaling pathway inhibition in MCF-7 and T47D cells, we blocked the TLR signaling pathway using OxPAPC, an antagonist of TLR signaling. Results: Among BC patients, miR-34a was down-regulated, CXCL10 was up-regulated, and the TLR signaling pathway was activated. Determination of luciferase activity revealed that CXCL10 was a target of miR-34a. Through gain- and loss-of-function studies, miR-34a was demonstrated to negatively regulate CXCL10; inhibit activation of the TLR signaling pathway; significantly suppress in vitro cell proliferation, migration, and invasion; and induce apoptosis. Conclusion: Our findings suggest that functional loss or suppression of the tumor suppressor CXCL10 due to induction of miR-34a leads to inhibition of the TLR signaling pathway during breast tumorigenesis, providing a novel target for the molecular treatment of breast malignancies.

show abstract

Section: Introductionmentioning

confidence: 99%

MicroRNA-34a Inhibition of the TLR Signaling Pathway Via CXCL10 Suppresses Breast Cancer Cell Invasion and Migration

Xu¹,

Liu²,

Yang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Expressions of Ki‐67 and SOX2 were evaluated using immunohistochemistry assay as previously described . Briefly, slides were washed with specific reagents in the following order: xylene, two times, 5 minutes each; 100% ethanol, two times, 5 minutes each, 95% ethanol, two times, 5 minutes each, 80% ethanol, once, 5 minutes; 70% ethanol, once, 5 minutes; 50% ethanol, once, 5 minutes; dH 2 O, two times, 5 minutes each.…”

Section: Methodsmentioning

confidence: 99%

“…Expressions of Ki-67 and SOX2 were evaluated using immunohistochemistry assay as previously described. 23 Briefly, slides were washed with specific reagents in the following order: xylene, two times, 5 minutes each; 100% ethanol, two times, 5 minutes each, 95%…”

Section: Immunohistochemistrymentioning

confidence: 99%

Downregulation of long non‐coding RNA Opa interacting protein 5‐antisense RNA 1 inhibits breast cancer progression by targeting sex‐determining region Y‐box 2 by microRNA‐129‐5p upregulation

et al. 2018

Self Cite

View full text Add to dashboard Cite

Several studies have shown an important role for long non‐coding RNA (lncRNA) in breast cancer progression. The present study investigated the role of lncRNA Opa interacting protein 5‐antisense RNA 1 (OIP5‐AS1) in the progression of breast cancer. OIP5‐AS1 was significantly upregulated in breast cancer tissues and in breast cancer cell lines, and OIP5‐AS1 downregulation inhibited the malignant behavior of breast cancer in vitro and in vivo. For in‐depth exploration of the mechanism of OIP5‐AS1 in breast cancer, we found that expression of microRNA‐129‐5p(miR‐129‐5p), which was found to bind sites in the sequence of OIP5‐AS1, in breast cancer tissues was negatively correlated with OIP5‐AS1. Also, luciferase assays indicated that OIP5‐AS1 acted as a miR‐129‐5p sponge, resulting in upregulated expression of the sex‐determining region Y‐box 2 (SOX2) transcription factor. Our study showed that OIP5‐AS1 plays a critical role in promoting breast cancer progression and that OIP5‐AS1 downregulation targets SOX2 by miR‐129‐5p upregulation.

show abstract

“…For instance, miR-129-5p was demonstrated to stimulate Her-2-positive breast cancer sensitive to trastuzumab [9]. MiR-212-5p/miR-101 was validated to exert inhibitory influences on breast cancer in some studies [10,11], while miR-1246 promoted breast cancer and its drug resistance, [12] and miR-181a had dual regulatory roles in BRCA [13]. The molecular regulatory network of BRCA is quite complex, and thus, the specific molecular mechanisms of BRCA progression remain to be further elaborated.…”

Section: Introductionmentioning

confidence: 99%

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Feng

Wang

Liang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Next-generation sequencing (NGS) has revealed abundant long noncoding RNAs (lncRNAs) that have been characterized as critical components of cancer biology in humans. The present study aims to investigate the role of the lncRNA KCNQ1OT1 in breast cancer (BRCA) as well as the underlying molecular mechanisms and functions of KCNQ1OT1 involved in the progression of BRCA. Methods: The Cancer Genome Atlas (TCGA) and StarBase v2.0 were used to obtain the required gene data. Dual luciferase reporter gene assays were conducted to verify the relevant intermolecular target relationships. QRT-PCR and Western blot were performed to measure the expression levels of different molecules. Cell proliferation was detected by using the MTT and colony formation assays, while cell migration and invasion were examined by transwell assay. Variations in cell apoptosis and cell cycle were determined through flow cytometry. A tumor xenograft model was applied to assess tumor growth in vivo. Results: KCNQ1OT1 was found to be remarkably highly expressed in BRCA tissues and cells. KCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2. Conclusion: The KCNQ1OT1/miR-145/CCNE2 axis plays a critical regulatory role in BRCA, potentially giving rise to BRCA tumorigenesis and progression. These findings provide valuable evidence for improving the diagnosis and treatment of BRCA in the future.

show abstract

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Cited by 44 publications

References 50 publications

MicroRNA-34a Inhibition of the TLR Signaling Pathway Via CXCL10 Suppresses Breast Cancer Cell Invasion and Migration

MicroRNA-34a Inhibition of the TLR Signaling Pathway Via CXCL10 Suppresses Breast Cancer Cell Invasion and Migration

Downregulation of long non‐coding RNA Opa interacting protein 5‐antisense RNA 1 inhibits breast cancer progression by targeting sex‐determining region Y‐box 2 by microRNA‐129‐5p upregulation

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Contact Info

Product

Resources

About