MiR-196a promoted cell migration, invasion and the epithelial-mesenchymal transition by targeting HOXA5 in osteosarcoma

2020 ◽  
Vol 29 (2) ◽  
pp. 291-298
Author(s):  
Xiaoli Wang ◽  
Lili Zhang ◽  
Xingfeng Zhang ◽  
Cuihong Xing ◽  
Ruidong Liu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Mesenchymal Transition ◽  
Bone Cancer ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Tumor Tissues ◽  
Cell Metastasis ◽  
Primary Bone ◽  
Polymerase Chain ◽  
Dual Luciferase Reporter Assay

INTRODUCTION: Osteosarcoma (OS), aggressive neoplasms of the bone, is the most common primary bone cancer in children. MiR-196a usually low expressed in several tumors and its functions in osteosarcoma still unclear. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess the expression of miR-196a and the HOXA5. Cell metastasis and epithelial-mesenchymal transition (EMT) abilities were assessed using Transwell and western blot. The dual luciferase reporter assay was carried out to verify whether miR-196a directly targeted the 3’-untranslated region (UTR) of HOXA5 mRNA. RESULTS: MiR-196a was overexpressed and HOXA5 was low expressed in osteosarcoma versus the non-tumor tissues and normal cell lines. Upregulation of miR-196a or downregulation of HOXA5 was associated with worse outcome of osteosarcoma patients. MiR-196a enhanced cell migration, invasion and EMT by regulating the expression of HOXA5 through directly targeting the 3’-UTR of its mRNA in osteosarcoma. HOXA5 partially reversed roles of miR-196a on metastasis and EMT in osteosarcoma. CONCLUSIONS: MiR-196a promoted cell metastasis and EMT by targeting the 3’-UTR of HOXA5 mRNA in osteosarcoma. The newly identified miR-196a/HOXA5 axis provides novel insight into the pathogenesis of osteosarcoma.

lncRNA NEAT1 Inhibits Proliferation, Invasion and Epithelial-mesenchymal Transition of Gastric Cancer Cells by Regulating MiR-129-5p/PBX3 Axis

2020 ◽  
Author(s):  
Hanshu Ji ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
Lncrna Neat1 ◽  
Dual Luciferase Reporter Assay

Abstract Purpose: lncRNA NEAT1 has been reported as a tumor-promoting gene in a variety of tumors, but few studies have explored its role and mechanism in gastric cancer. In the face of increasing incidence of gastric cancer, how to improve the diagnostic accuracy and therapeutic effect of gastric cancer is a major clinical problem. Therefore, we studied the effect and mechanism of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition of gastric cancer cells. To inquiry into the effect of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) cells by regulating miR-129-5p/PBX3 axis. Methods: Totally 63 GC diagnosed and treated in our hospital were selected as the study subjects, whose paired GC tissues and pericarcinomatous tissues were collected as the study specimens after obtaining their consent. QRT-PCR was employed to detect the NEAT1 expression in tissues and cells to analyze the relationship between NEAT1 and clinicopathological data of GC patients. In addition, stable and transient overexpression and inhibition vectors were established and transfected into GC cells HCG-27 and MKN-45. CCK-8, traswell, and flow cytometry were employed to evaluate the proliferation, invasion, and apoptosis of transfected cells. The correlation of miR-129-5p between PBX3 and NEAT1 was assessed using dual luciferase reporter assay, while that between NEAT1 and miR-129-5p was assessed by RNA-binding protein immunoprecipitation (RIP) . Western blot was applied for the detection of apoptosis and EMT related proteins.Results: NEAT1 was overexpressed in GC patients and had a high diagnostic value. The expression of NEAT1 was related to the pathological stage, differentiation degree, tumor size and lymph node metastasis of patients with GC. Down-regulated NEAT1 brought decreased cell proliferation, invasion and EMT, and increased apoptosis. According to dual luciferase reporter assay, NEAT1 could target miR-129-5p, while in turn miR-129-5p could target PBX3. Functional analysis exhibited that miR-129-5p overexpression inhibited PBX3 in GC cells, affecting cell proliferation, invasion, EMT and apoptosis, and rescue experiments demonstrated that these effects were eliminated by up-regulating NEAT1 expression.Conclusion: Inhibition of NEAT1 could mediate miR-129-5p/PBX3 axis to promote apoptosis of GC cells, and reduce cell proliferation, invasion and EMT.

scholarly journals lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

2018 ◽  
Vol 48 (5) ◽  
pp. 1928-1941 ◽  
Author(s):  
Chuan He ◽  
Zhigang Liu ◽  
Li Jin ◽  
Fang Zhang ◽  
Xinhao Peng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

scholarly journals FoxM1 affects adhesive, migratory, and invasive abilities of human retinoblastoma Y-79 cells by targeting matrix metalloproteinase 2

2020 ◽  
Vol 52 (3) ◽  
pp. 294-301
Author(s):  
Xue Zhu ◽  
Mengxi Yu ◽  
Ke Wang ◽  
Wenjun Zou ◽  
Ling Zhu
Keyword(s):  
Matrix Metalloproteinase ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Matrix Metalloproteinase 2 ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Forkhead Box ◽  
Cell Metastasis ◽  
Human Retinoblastoma ◽  
Novel Target

Abstract Forkhead box protein M1 (FoxM1) is an important transcription factor involved in various pathological processes including tumor metastasis. The changes of adhesive, migratory, and invasive abilities are considered as crucial events in tumor metastasis progression. In this study, we aimed to investigate the correlation between FoxM1 and retinoblastoma (Rb) metastasis and to explore the detailed mechanism. Wound healing, cell adhesion, and invasion assays showed that FoxM1 overexpression induced epithelial–mesenchymal transition in Y-79 cells and inhibited adhesion and subsequently promoted metastasis of Y-79 cells, while FoxM1 knockdown showed the opposite effects. A luciferase reporter assay and chromatin immunoprecipitation assay provided evidence that FoxM1 promoted matrix metalloproteinase 2 (MMP2) transcription by directly binding to and promoting MMP2 promoter. MMP2 knockdown by siRNA transfection attenuated cell metastasis of Y-79 cells induced by FoxM1 overexpression. Furthermore, the FoxM1-binding site mapped between −1167 and −1161 bp of the MMP2 promoter was identified. Our results suggested that the FoxM1–MMP2 axis plays an important role in Rb metastasis, which may be a novel target for designing therapeutic regimen to control Rb metastasis.

scholarly journals MiR-199a-3p/5p participate in TGF-β and EGF induced EMT in pterygium by targeting DUSP5/MAP3K11

2020 ◽  
Author(s):  
Siying He ◽  
Yifang Huang ◽  
Shiqi Dong ◽  
Chen Qiao ◽  
Guohua Yang ◽  
...  
Keyword(s):  
Target Genes ◽  
Epithelial Mesenchymal Transition ◽  
Cell Model ◽  
Luciferase Reporter ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling ◽  
Emt Markers ◽  
Dual Luciferase Reporter Assay

Abstract Background: Recently, it has been reported that miRNA is correlated with pterygium, however its exact mechanism in pterygium is unrevealed and require further investigation. Methods: The differential expression of miRNA in pterygium was profiled using microarray and validated with quantitative real-time PCR (qRT-PCR). Human conjunctival epithelial cells (HCEs) were cultured and treated with TGF-b and EGF. Western blot and immunohistochemistry were carried out to detect epithelial-mesenchymal transition (EMT) markers. Wound healing and transwell assay were used to determine cell migration ability, while apoptosis was determined by flow cytometry. The target genes of miR-199a were confirmed by the dual-luciferase reporter assay. Results: TGF-b and EGF induced EMT in HCEs to mimic the pathogenesis of pterygium. MiR-199a-3p and miR-199a-5p induced EMT in HCEs, whose respectively downstream targets DUSP5 and MAP3K11 hindered EMT in EMT-HCEs in turn. TGF-b and EGF induced EMT promotion and target genes suppression, could be promoted by miR-199a-3p and miR-199a-5p, while impeded by miR-199a-3p and miR-199a-5p inhibitors. The expression levels of miR-199a and target genes were further validated in pterygium tissues, which were consistent the results in cell model. Bioinformatics analysis indicated the miR-199a-3p/5p-DUSP5/MAP3K11 was belong to MAPK signalling pathway in pterygium. Conclusions: TGF-b and EGF probably induced EMT of HCEs through miR-199a-3p/5p-DUSP5/MAP3K11 axis, which explained the pathogenesis of EMT in pterygium and might provide new targets for pterygium prevention and therapy.

scholarly journals MiR-200b Suppresses Gastric Cancer Cell Migration and Invasion by Inhibiting NRG1 through ERBB2/ERBB3 Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Tonglei Xu ◽  
Fangliang Xie ◽  
Dazhou Xu ◽  
Weidong Xu ◽  
Xuming Ge ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Neuregulin 1 ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Erbb3 Signaling

Purpose. Accumulating evidence indicates that miRNAs (miRs) play crucial roles in the modulation of tumors development. However, the accurately mechanisms have not been entirely clarified. In this study, we aimed to explore the role of miR-200b in the development of gastric cancer (GC). Methods. Western blot and RT-PCR were applied to detect epithelial-mesenchymal transition (EMT) marker expression and mRNA expression. Transwell assay was used for measuring the metastasis and invasiveness of GC cells. TargetScan system, luciferase reporter assay, and rescue experiments were applied for validating the direct target of miR-200b. Results. MiR-200b was prominently decreased in GC tissues and cells, and its downregulation was an indicator of poor prognosis of GC patients. Reexpression of miR-200b suppressed EMT along with GC cell migration and invasion. Neuregulin 1 (NRG1) was validated as the target of miR-200b, and it rescued miR-200b inhibitory effect on GC progression. In GC tissues, the correlation of miR-200b with NRG1 was inverse. Conclusion. MiR-200b suppressed EMT-related migration and invasion of GC through the ERBB2/ERBB3 signaling pathway via targeting NRG1.

scholarly journals Circ_0000215 Increases the Expression of CXCR2 and Promoted the Progression of Glioma Cells by Sponging miR-495-3p

2020 ◽  
Vol 19 ◽  
pp. 153303382095702
Author(s):  
Nurehemaiti Mutalifu ◽  
Peng Du ◽  
Jingjing Zhang ◽  
Halik Akbar ◽  
Baofeng Yan ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Glioma Cells ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Mesenchymal Transition ◽  
Polymerase Chain ◽  
The Relationship ◽  
Rip Assay ◽  
Competitive Endogenous Rna

Background: In recent years, accumulating studies have found that circular RNA (circRNA) exerts a great effect on tumor progression. Circ_0000215, a novel circRNA, remains largely unknown in terms of its effect and mechanism in glioma. Method: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to detect the expressions of circ_0000215, miR-495-3p and CXCR2 in human glial cell line HEB and glioma cell lines (A172, U251, U87, SHG-44, LN-18), human glioma tissues and adjacent healthy tissues. Gain- and loss-assays of circ_0000215 were conducted. Cell proliferation ability was detected via the CCK8 assay, and cell invasion ability was examined by Transwell assay. CXCR2 expression was evaluated via RT-PCR and Western blot. Moreover, bioinformatics was applied to analyze the targeting molecules of circ_0000215 and CXCR2. Verification of the relationship between these molecules were supported through the dual-luciferase reporter gene and RNA immunocoprecipitation (RIP) assay. Results: Circ_0000215 and CXCR2 were remarkably upregulated in glioma tissues and cells. Overexpression of circ_0000215 notably promoted the proliferation, invasion and epithelial-mesenchymal transition (EMT) but inhibited apoptosis of glioma cells, while knocking down circ_0000215 had the opposite effects. Additionally, miR-495-3p, a sponge RNA of circ_0000215, inhibited the growth, invasion and EMT of glioma cells. Mechanistically, miR-495-3p targeted CXCR2 and negatively regulated CXCR2/PI3K/Akt pathway. However, the effects of miR-495-3p were all dampened by overexpression of circ_0000215. Conclusion: These data demonstrated that circ_0000215 functions as a competitive endogenous RNA by sponging miR-495-3p, thus accelerating glioma progression through CXCR2 axis.

scholarly journals MiR-199a-3p/5p participated in TGF-β and EGF induced EMT by targeting DUSP5/MAP3K11 in pterygium

2020 ◽  
Author(s):  
Siying He ◽  
Yifang Huang ◽  
Shiqi Dong ◽  
Chen Qiao ◽  
Guohua Yang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Luciferase Reporter ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Investigation Methods

Abstract Background Recently, it has been reported that miRNA is involved in pterygium, however the exact underlying mechanism in pterygium is unrevealed and require further investigation. Methods The differential expression of miRNA in pterygium was profiled using microarray and validated with quantitative real-time polymerase chain reaction(qRT-PCR). Human conjunctival epithelial cells (HCEs) were cultured and treated with transforming growth factor β (TGF-β) and epidermal growth factor (EGF) and transfected with miR-199a-3p/5p mimic and inhibitor. Markers of epithelial-mesenchymal transition (EMT) in HCEs were detected using western blot and immunohistochemistry. Cell migration ability was determined using wound healing and transwell assay, while apoptosis was determined by flow cytometry. The target genes of miR-199a were confirmed by the dual-luciferase reporter assay. Results TGF-β and EGF could induced EMT in HCEs and increase miR-199a-3p/5p but suppress target genes, DUSP5 and MAP3K11. With the occurrence of EMT, cell migration ability was enhanced, and apoptosis was impeded. Promoting miR-199a-3p/5p expression could induce EMT in HCEs without TGF-β and EGF, while suppressing miR-199a-3p/5p could inhibit EMT in TGF-β and EGF induced HCEs. In a word, TGF-β and EGF induced EMT could be regulated with miR-199a-3p/5p-DUSP5/MAP3K11 axes. The validated results in tissues showed that, compared with control conjunctival tissues, miR-199a-3p/5p were more overexpressed in pterygium, while DUSP5/MAP3K11 were lower expressed. In addition, bioinformatics analysis indicated the miR-199a-3p/5p-DUSP5/MAP3K11 was belong to MAPK signalling pathway. Conclusions TGF-β and EGF induce EMT of HCEs through miR-199a-3p/5p-DUSP5/MAP3K11 axes, which explains the pathogenesis of EMT in pterygium and may provide new targets for pterygium prevention and therapy.

scholarly journals Gly-tRF enhances LCSC-like properties and promotes HCC cells migration by targeting NDFIP2

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yongqiang Zhou ◽  
Jinjing Hu ◽  
Lu Liu ◽  
Mengchao Yan ◽  
Qiyu Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Pathway Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Flow Cytometric Analysis ◽  
Signalling Pathway ◽  
Luciferase Reporter ◽  
Mesenchymal Transition ◽  
Phosphorylated Akt ◽  
Sphere Formation

Abstract Background Accumulating evidence demonstrates that tRFs (tRNA-derived small RNA fragments) and tiRNAs (tRNA-derived stress-induced RNA), an emerging category of regulatory RNA molecules derived from transfer RNAs (tRNAs), are dysregulated in in various human cancer types and play crucial roles. However, their roles and mechanisms in hepatocellular carcinoma (HCC) and liver cancer stem cells (LCSCs) are still unknown. Methods The expression of glycine tRNA-derived fragment (Gly-tRF) was measured by qRT-PCR. Flow cytometric analysis and sphere formation assays were used to determine the properties of LCSCs. Transwell assays and scratch wound assays were performed to detect HCC cell migration. Western blotting was conducted to evaluate the abundance change of Epithelial-mesenchymal transition (EMT)-related proteins. Dual luciferase reporter assays and signalling pathway analysis were performed to explore the underlying mechanism of Gly-tRF functions. Results Gly-tRF was highly expressed in HCC cell lines and tumour tissues. Gly-tRF mimic increased the LCSC subpopulation proportion and LCSC-like cell properties. Gly-tRF mimic promoted HCC cell migration and EMT. Loss of Gly-tRF inhibited HCC cell migration and EMT. Mechanistically, Gly-tRF decreased the level of NDFIP2 mRNA by binding to the NDFIP2 mRNA 3′ UTR. Importantly, overexpression of NDFIP2 weakened the promotive effects of Gly-tRF on LCSC-like cell sphere formation and HCC cell migration. Signalling pathway analysis showed that Gly-tRF increased the abundance of phosphorylated AKT. Conclusions Gly-tRF enhances LCSC-like cell properties and promotes EMT by targeting NDFIP2 and activating the AKT signalling pathway. Gly-tRF plays tumor-promoting role in HCC and may lead to a potential therapeutic target for HCC.

scholarly journals Upregulation of circRNA hsa_circ_0008726 in Pre-eclampsia Inhibits Trophoblast Migration, Invasion, and EMT by Regulating miR-345-3p/RYBP Axis

2021 ◽  
Author(s):  
Chang Shu ◽  
Peng Xu ◽  
Jun Han ◽  
Shumei Han ◽  
Jin He
Keyword(s):  
Cell Migration ◽  
Epithelial Mesenchymal Transition ◽  
Extravillous Trophoblast ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rnase R ◽  
Mesenchymal Transition ◽  
Potential Biomarker ◽  
Rna Immunoprecipitation

AbstractAccumulating evidence shows that impaired spiral artery remodeling, placental dysfunction, and insufficient trophoblast infiltration contribute to the etiology and pathogenesis of pre-eclampsia (PE). circRNAs are a class of endogenous non-coding RNAs implicated in the pathogenesis of many diseases, including PE. This study aims to investigate the role of circRNA hsa_circ_0008726 in regulating the migration and invasion of extravillous trophoblast cells. RNase R assay was performed to confirm that circ_0008726 was a circular transcript. The expression of circ_0008726, RYBP, and miR-345-3p was examined by qRT-PCR. The functional interaction between miR-345-3p and circ_0008726 or RYBP was confirmed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Cell migration and invasion ability was analyzed by Transwell assays. Western blot was used for the quantification of RYBP protein level. Circ_0008726 expression was significantly increased in PE placenta tissues as compared with normal placenta tissues. Circ_0008726 was resistant to RNase R digestion and was predominately located in the cytoplasm of HTR-8/SVneo cells. Silencing circ_0008726 promoted cell migration and EMT (epithelial-mesenchymal transition), while circ_0008726 overexpression suppressed these processes. Mechanistically, circ_0008726 sponged miR-345-3p to negatively regulate its expression, and miR-345-3p negatively modulated the expression of RYBP. In PE samples, the expression level of circ_0008726 was negatively correlated with miR-345-3p level, but was positively correlated with RYBP expression. Transfection of miR-345-3p mimic or RYBP knockdown counteracted the effects of circ_0008726 overexpression on cell migration and EMT. Our data demonstrate the upregulation of circ_0008726 in PE placenta, which inhibits the migration, invasion, and EMT of HTR-8/SVneo cells by targeting miR-345-3p/RYBP axis. These data suggest that circ_0008726 could be a potential biomarker and therapeutic target for PE.

scholarly journals MicroRNA-296-5p inhibits cell metastasis and invasion in nasopharyngeal carcinoma by reversing transforming growth factor-β-induced epithelial–mesenchymal transition

2020 ◽  
Vol 25 (1) ◽  
Author(s):  
Meihui Chen ◽  
Chen Chen ◽  
Haiqing Luo ◽  
Jing Ren ◽  
Qiuqin Dai ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Real Time ◽  
Real Time Pcr ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Metastasis

Abstract Aim To explore the effect of miR-296-5p on the metastasis of nasopharyngeal carcinoma (NPC) cells and investigate the underlying mechanism. Methods The expressions of miR-296-5p in NPC tissues and cells were determined using GSE32920 database analysis and real-time PCR and miRNA microarray assays. An miR-296-5p mimic and inhibitor were transfected into NPC cells. Then, immunofluorescence imaging, scratch wound-healing, transwell migration and invasion assays were used to observe the effects of miR-296-5p on cell metastasis and invasion. Real-time PCR and western blotting were carried out to detect the expressions of genes and proteins related to epithelial–mesenchymal transition (EMT). A dual luciferase reporter assay was used to identify whether TGF-β is the target gene of miR-296-5p. Finally, TGF-β expression plasmids were transfected into NPC cells to verify the role of TGF-β in the miR-296-5p-mediated inhibition of nasopharyngeal carcinoma cell metastasis. Results Our results show that miR-296-5p inhibits the migratory and invasive capacities of NPC cells by targeting TGF-β, which suppresses EMT. Importantly, the miR-296-5p level was significantly lower in human NPC tissues than in adjacent normal tissues. It also negatively correlated with TGF-β and was significantly associated with the lymph node metastasis of patients with NPC. Conclusions Our findings show that miR-296-5p represses the EMT-related metastasis of NPC by targeting TGF-β. This provides new insight into the role of miR-296-5p in regulating NPC metastasis and invasiveness.

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