MiRNA-34a reversed TGF-β-induced epithelial-mesenchymal transition via suppression of SMAD4 in NPC cells

Huang, Guanhong; Du, Mengnan; Zhu, Hongming; Zhang, Nan; Lü, Zhiwei; Qian, Lu‐Xi; Zhang, Wenjun; Tian, Xiaokang; He, Xia; Li, Yin

doi:10.1016/j.biopha.2018.06.115

Cited by 49 publications

(36 citation statements)

References 31 publications

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“…miR-34a-5p by targeting Smad family member 4 (Smad4) can regulate cancer cell migration and invasion. 118,119 In PE patients, miR-34a-5p was significantly increased compared with normal group. 96 Moreover, the upregulation of miR-34a-5p remarkably inhibited the migration of trophoblast cell line (HTR8/SVnevo) by targeting Smad4 and transfected miR-34a-5p inhibitor elevated invasion of HTR8/SVnevo.…”

Section: Targeting Smad Family Membermentioning

confidence: 88%

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The role of epigenetic changes in preeclampsia

et al. 2019

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Preeclampsia (PE) is a disorder affecting 2–10% of pregnancies and has a major role for perinatal and maternal mortality and morbidity. PE can be occurred by initiation of new hypertension combined with proteinuria after 20 weeks gestation, as well as various reasons such as inflammatory cytokines, poor trophoblast invasion can be related with PE disease. Environmental factors can cause epigenetic changes including DNA methylation, microRNAs (miRNAs), and histone modification that may be related to different diseases such as PE. Abnormal DNA methylation during placentation is the most important epigenetic factor correlated with PE. Moreover, changes in histone modification like acetylation and also the effect of overregulation or low regulation of miRNAs or long noncoding RNAs on variety signaling pathways can be resulted in PE. The aim of this review is to describe of studies about epigenetic changes in PE and its therapeutic strategies.

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Section: Targeting Smad Family Membermentioning

confidence: 88%

“…miR‐34a‐5p by targeting Smad family member 4 (Smad4) can regulate cancer cell migration and invasion . In PE patients, miR‐34a‐5p was significantly increased compared with normal group .…”

Section: Epigenetic Changes In Pementioning

confidence: 99%

The role of epigenetic changes in preeclampsia

et al. 2019

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“…It indicated that miR-34 acted as a tumor suppressor in NPC, and may be a novel therapeutic target for the treatments of patients with NPC. 45 Moreover, over-expression of miR-425 is induced by IL-1b, which aim at 3 0 UTR of miR-425, could regulate homolog expression of tensin and phosphatase. The activation of NF-kB induced by IL-1b up-regulates miR-425 expression, while enhances transcription of miR-425 gene.…”

Section: Discussionmentioning

confidence: 99%

miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway

Liu

Chen

2019

RSC Adv.

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Background: EMT has a crucial effect on the progression and metastasis of tumors. This work will elucidate the role of miR-425 in EMT and the development of TNBC. Methods: The differential miRNA expression among non-tumor, para-tumor (adjacent tissue of tumor) and tumor tissues was analyzed. The luciferase activities of TGF-b1 3 0 UTR treated with miR-425 were determined. Then human breast cancer cell lines were treated with mimics or inhibitors of miR-425, and then the cell proliferation and migration, and invasion ability were assessed. The expression of TGF-b1 and markers of epithelial cells and mesenchymal cells were analyzed. The influences of miR-425 on the development of TNBC through inducing EMT by targeting the TGF-b1/SMAD3 signaling pathway in TNBC cell lines were investigated. Furthermore, xenograft mice were used to explore the potential roles of miR-425 on EMT and the development of TNBC in vivo. Results: Compared with non-tumor tissues, 9 miRNAs were upregulated and 3 miRNAs were down-regulated in tumor tissues. The relative expression of miR-425 in tumor tissues was obviously much lower than that in para-tumor and non-tumor tissues. MiR-425 suppressed TGF-b1 expression, and further inhibited expression of mesenchymal cell markers, while it exerted effects on cell proliferation and migration of TNBC cell lines. Moreover, the agomir of miR-425 could protect against the development process in a murine TNBC xenograft model. Conclusions: Our results demonstrated that miR-425 targets TGF-b1, and was a crucial suppressor on EMT and the development of TNBC through inhibiting the TGF-b1/SMAD3 signaling pathway. This suggests that aiming at the TGF-b1/SMAD3 signaling pathway by enhancing relative miR-425 expression, is a feasible therapy strategy for TNBC. RNA extractionTRIzol method was used to extract total RNA from tissues based on the operation manual. Then, smaller RNA (<200 nt) was removed with mirVana RNA isolation kit (Cat. no. AM27828; Invitrogen Thermo Fisher Scientic, Inc., Waltham, MA, USA) according to the instructions for manufacturer. Culture of cellThe cell lines of human TNBC, including MDA-MB-231 (ATCC® HTB-26™) and Hs 578T (ATCC® HTB-126™) were purchased from ATCC (American Type Culture Collection), and then cultured in DMEM with 10% FBS accompanied by Streptomycin and Penicillin (bi-antibiotics) with atmosphere (5% CO 2 ) at 37 C. siRNA for TGF-b1The well known siRNA of TGF-b1 supported by ref. 26 had been used in our study, which had been used as a positive in our study. The siRNA duplexes for TGF-b1 sequences are 5 0 -152 | RSC Adv., 2019,9,[151][152][153][154][155][156][157][158][159][160][161][162][163][164][165] This journal is Fig. 8 MiR-425 suppressed cell invasion of TNBC cell lines. Moreover, the inhibitors of miR-425 promoted invasion ability of TNBC cell lines, but the mimics of miR-425 suppressed the invasion ability of TNBC cell lines.This journal is Fig. 9 MiR-425 agomir suppressed TNBC xenografts. To detect anti-tumor activity induced by miR-425 agomir in vivo, human TNBC ...

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“…EC‐1 cell lines were starved overnight before treatment. To stimulate cells with TGF‐β1 (R&D Systems, USA), these cells were incubated with 1% FBS containing 10 ng/mL TGF‐β1 for 48 hours to reach the EMT state …”

Section: Methodsmentioning

confidence: 99%

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

Tian

Qian

et al. 2019

Cancer Medicine

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Metastasis and invasion are the primary causes of malignant progression in esophageal squamous cell carcinoma (ESCC). Epithelial‐mesenchymal transition (EMT) is crucial step of acquisition of "stemness" properties in tumor cells. However, the mechanism of esophageal cancer metastasis remains unclear. This research was designed to explore the role and mechanism of SMAD4 and miR‐130a‐3p in the progression of transforming growth factor‐β (TGF‐β)‐induced EMT in vivo and in vitro. The expression of miR‐130a‐3p in ESCC cell line and normal esophageal epithelial cell was determined by RT‐qPCR. The protein expression levels of TGF‐β‐induced changes in EMT were analyzed by western blotting and immunofluorescence. Dual‐luciferase report assays were used to validate the regulation of miR‐130a‐3p‐SMAD4 axis. The effect of miR‐130a‐3p and SMAD4 in TGF‐β‐induced migration, invasion in the ESCC cell line EC‐1 was investigated by wound healing assays and Transwell assays. Here we found that knocked down SMAD4 could partially reverse TGF‐β‐induced migration, invasion, and EMT progression in the ESCC cell line EC‐1. miR‐130a‐3p, which directly targets SMAD4, is down‐regulated in ESCC. miR‐130a‐3p inhibits the migration and invasion of EC‐1 cells both in vitro and in vivo. Finally, miR‐130a‐3p inhibits TGF‐β‐induced EC‐1 cell migration, invasion, and EMT progression in a SMAD4‐dependent way. In conclusion, this study provides new insights into the mechanism underlying ESCC metastasis. The TGF‐β/miR‐130a‐3p/SMAD4 pathway could be potential targets for clinical treatment of ESCC.

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MiRNA-34a reversed TGF-β-induced epithelial-mesenchymal transition via suppression of SMAD4 in NPC cells

Cited by 49 publications

References 31 publications

The role of epigenetic changes in preeclampsia

The role of epigenetic changes in preeclampsia

miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway

miR‐130a‐3p regulated TGF‐β1‐induced epithelial‐mesenchymal transition depends on SMAD4 in EC‐1 cells

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