miR-145 inhibits proliferation and migration of breast cancer cells by directly or indirectly regulating TGF-β1 expression

Ding, Yongsheng; Zhang, Chunfu; Zhang, Jiahui; Zhang, Nannan; Li, Tao; Fang, Jie; Zhang, Yi; Zuo, Feiyang; Tao, Zehua; Tang, Shengnan; Zhu, Wei; Chen, Huabiao; Sun, Xiaochun

doi:10.3892/ijo.2017.3945

Cited by 75 publications

(70 citation statements)

References 35 publications

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“…Moreover, cancer cells silenced with siRNA against COL5A1 showed reduced cell invasion, demonstrating the association of higher COL5A1 expression with metastasis in many tumors including our TSCC patients . Previous studies showed that low expression of miR‐145 is associated with cell proliferation and migration in a wide variety of tumors and co‐expression of higher COL5A1 and low miR‐145 was detected in primary meningioma tissues, representing an indirect effect on COL5A1 transcriptional regulation . Regulation of COL5A1 by miR‐145 will need to be further verified in TSCC.…”

Section: Discussionmentioning

confidence: 74%

Differential clinical significance of COL5A1 and COL5A2 in tongue squamous cell carcinoma

Chen

Tseng

Shu

et al. 2019

J Oral Pathology Medicine

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Background Type V collagen (COL5), in the functional heterotrimer [α1(V)2α2(V)] isoform, participates in the malignancies of various cancers. However, its role in tongue squamous cell carcinoma (TSCC) remains unclear. Materials and Methods The expression levels of COL5A1 and COL5A2 polypeptide chains were examined using the tissue microarray from 245 TSCC patients with immunohistochemistry. Paired t test and Wilcoxon signed‐rank test were performed for comparisons among the groups. Survival rates were estimated by using the Kaplan‐Meier method and compared with log‐rank tests. A Cox proportional hazards model was used to evaluate the impact of protein expression level on survival rate. Results Expression level of COL5A1 was significantly increased in tumor tissues (P < 0.001) compared to that in corresponding adjacent normal tissues. High expression level of COL5A1 was associated with advanced pathological stage (III, IV, P = 0.015) and lymph node metastasis (P = 0.005) of TSCC patients. High expression level of COL5A1 was also correlated with poor disease‐specific survival (DSS, P = 0.001) and disease‐free survival (DFS, P = 0.003) in TSCC patients. However, high expression level of COL5A2 was correlated with better DFS in TSCC patients (P = 0.043). Moreover, co‐expression level of high (COL5A1)2/low (COL5A2) heterotrimer was correlated with worse DSS (P = 0.004) and DFS (P = 0.004). Conclusion COL5A1 is an unfavorable factor for tumorigenesis, clinicopathological outcomes, and prognosis, whereas COL5A2 is only a favorable factor for prognosis in TSCC. The co‐expression of high (COL5A1)2/low (COL5A2) heterotrimer is a more potential unfavorable factor for prognosis in TSCC.

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Section: Discussionmentioning

confidence: 74%

Differential clinical significance of COL5A1 and COL5A2 in tongue squamous cell carcinoma

Chen

Tseng

Shu

et al. 2019

J Oral Pathology Medicine

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“…miR‐145 is a newly discovered miRNA, which is significantly less expressed in breast cancer (Ding et al, ), cervical cancer (Sathyanarayanan et al, ), glioma (Xu et al, ), colon cancer (Li et al, ), esophageal cancer (Zhang et al, ), and non‐small‐cell lung cancer (Yin et al, ). The genes regulated by miRNA‐145 are different in different tumors, and the molecular mechanisms of their anti‐cancer effects are also different.…”

Section: Discussionmentioning

confidence: 99%

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

et al. 2019

Cell Biology International

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miR‐145 has been found to be a participant in cancer metastasis and glucose metabolism in ovarian cancer. However, the role of glutamine metabolism in ovarian cancer remains unclear. In this study, we aim to elucidate the molecular mechanism underlying the regulation of glutamine metabolism by miR‐145 in ovarian cancer cells. The messenger RNA (mRNA) levels of miR‐145 and glutaminase 1 (GLS1) were examined by quantitative real‐time polymerase chain reaction (qRT‐PCR). The protein levels of c‐myc and GLS1 were detected by western blot analysis. Luciferase reporter assays were used to validate c‐myc was a target of miR‐145. Glutamine metabolism was analyzed using assay kits. In addition, we performed luciferase reporter assays and chromatin immunoprecipitation assay to validate c‐myc transcription activated GLS1 and promoted GLS1 expression. The qRT‐PCR demonstrated that the mRNA level of miR‐145 and GLS1 was negatively correlated in ovarian cancer tissues and cell lines. Kaplan–Meier survival analysis and the log‐rank test showed that patients with high miR‐145 expression had significantly increased the overall survival. The overexpression of miR‐145 inhibited glutamine consumption, α‐ketoglutarate production, and cellular ATP levels. Furthermore, we found miR‐145 inhibited glutamine metabolism by targeting c‐myc. Moreover, c‐myc could promote GLS1 expression by transcription activated. Together, our results revealed that miR‐145 inhibited glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells, which may improve the current strategy of ovarian cancer diagnosis and therapy.

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“…Zhang et al verified that miR-145 acts as a tumor suppressor and that its downregulation in tumor tissues may contribute to the progression of BRCA through a mechanism involving ROCK1 [28]. Ding et al suggested that miR-145 may inhibit TGF-beta1 protein expression, which may in turn induce the initiation and progression of BRCA [29]. In this research, miR-145 was found to be expressed at notably low levels in BRCA tissues and cells, and overexpression of miR-145 remarkably promoted cell apoptosis in BRCA by regulating CCNE2.…”

Section: Discussionmentioning

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

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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.

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miR-145 inhibits proliferation and migration of breast cancer cells by directly or indirectly regulating TGF-β1 expression

Cited by 75 publications

References 35 publications

Differential clinical significance of COL5A1 and COL5A2 in tongue squamous cell carcinoma

Differential clinical significance of COL5A1 and COL5A2 in tongue squamous cell carcinoma

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

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

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