MicroRNA-148b suppresses proliferation, migration, and invasion of nasopharyngeal carcinoma cells by targeting metastasis-associated gene 2

Wu, Ming‐Chi; Ye, Xiaoxia; Wang, Sheng-Chun; Li, Qinghua; Lai, Yue‐Yun; Yi, Yanmei

doi:10.2147/ott.s135664

Cited by 16 publications

(8 citation statements)

References 25 publications

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“…Further investigations are needed to reveal their functions and mechanisms in NPC tumorigenesis. Some of the NPC-related miRNAs found in previous studies were not identified in this study, including targeting of STAT3 by miRNA-98, targeting of TGF β R2 by miR-93, and targeting of metastasis-associated gene 2 by miRNA-148b [ 44 – 46 ]. These partially inconsistent results may reflect differences in sample types, screening tools, or quantification methods.…”

Section: Discussionmentioning

confidence: 70%

Dynamic Changes in Plasma MicroRNAs Have Potential Predictive Values in Monitoring Recurrence and Metastasis of Nasopharyngeal Carcinoma

Xu¹,

Lü

Fan

et al. 2018

BioMed Research International

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Although circulating microRNAs (miRNAs) have already proven to be useful as diagnostic and prognostic biomarkers in nasopharyngeal carcinoma (NPC), the potential of these molecules to monitor patients over time has been less explored. This study aimed to analyze dynamic changes in plasma miRNAs before and after treatment and explore their clinical significance in monitoring recurrence and metastasis of NPC. Candidate miRNAs were screened by microarray analysis and validated by real-time quantitative polymerase chain reaction (RT-qPCR). In the follow-up cohort including 102 patients, blood samples (plasma) were collected before the treatment initiation, 3 months, 6 months, and 12 months after treatments, and at the time of any recurrence or metastasis. Among these plasma miRNAs, miR-9-3p, miR-124-3p, miR-892b, and miR-3676-3p were significantly upregulated (P = 0.018, P = 0.039, P = 0.001, and P = 0.01, resp.) after treatment compared with pretreatment, and the four plasma miRNAs were downregulated again at recurrence or metastasis (P < 0.001, P = 0.015, P = 0.003, and P = 0.026, resp.). The dynamic changes in plasma miRNAs after treatment reflect the outcome of the disease and have the potential to monitor recurrence and metastasis in patients with NPC.

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Section: Discussionmentioning

confidence: 70%

Dynamic Changes in Plasma MicroRNAs Have Potential Predictive Values in Monitoring Recurrence and Metastasis of Nasopharyngeal Carcinoma

Xu¹,

Lü

Fan

et al. 2018

BioMed Research International

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“…Several miRNAs have been reported to serve as oncogenes or suppressor genes in NPC cell migration, invasion and metastasis. These miRNAs include miR-145 [8], miR-429 [9], miR-143 [10] and miR-148-b [11]. These studies suggest that miRNAs play important roles in NPC and provide a novel area of study in NPC invasion and metastasis.…”

Section: Introductionmentioning

confidence: 83%

miR-184 Inhibits Tumor Invasion, Migration and Metastasis in Nasopharyngeal Carcinoma by Targeting Notch2

Zhu¹,

Jiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: A recent study found that dysregulated microRNA-184 (miR-184) is involved in the proliferation and survival of nasopharyngeal carcinoma (NPC). This study aimed to evaluate the detailed mechanisms of invasion, migration and metastasis of NPC cells. Methods: Quantitative reverse-transcription PCR (qRT-PCR) and Western blot were used to confirm the expression levels of miR-184 and Notch2. NPC cell invasion and migration were subsequently examined using in vitro cell invasion and wound-healing assays, respectively. MicroRNA (miRNA) target gene prediction databases and dual-luciferase reporter assay were adopted to validate the target genes of miR-184. Results: MiR-184 was downregulated in the NPC cell lines. The miR-184 inhibitor increased the number of invading NPC cells, whereas miR-184 mimics inhibited the invasive ability of such cells. The protein level of E-cadherin decreased, whereas those of N-cadherin and vimentin increased in the anti-miR-184 group. This result showed that miR-184 inhibited NPC cell invasion and metastasis by regulating EMT progression. MiRNA target gene prediction databases indicated the potential of Notch2 as a direct target gene of miR-184. Such a notion was then validated by results of dual-luciferase reporter assay. Notably, shRNANotch2 restrained the EMT and partially abrogated the inhibitory effects of miR-184 on EMT progression in NPC cells. Conclusion: MiR-184 functions as a tumour-suppressive miRNA targeting Notch2 and inhibits the invasion, migration and metastasis of NPC.

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“…Excessive migration and invasion of tumor cells is recognized as the first step of neoplasm metastasis. 19 , 20 The effect of decreased Nodal expression on cell migration and invasion was determined by transwell assay. Our results demonstrated that downregulation of Nodal significantly inhibited the cell migration and invasion capabilities of bladder cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Nodal regulates bladder cancer cell migration and invasion via the ALK/Smad signaling pathway

Zhong

Zhu

et al. 2018

OTT

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BackgroundBladder cancer is the most common malignant tumor of the urinary tract. We aimed to explore the biological role and molecular mechanism of Nodal in bladder cancer.Materials and methodsThe expression of Nodal in bladder cancer tissues and cells was determined by quantitative real-time polymerase chain reaction. The effect of silencing of Nodal on cell proliferation, clone formation, and migration and invasion was evaluated by MTT cell proliferation assay, colony formation, and transwell assays, respectively. Western blot analysis was employed to detect the expression of proliferation- and invasion-related proteins and proteins involved in ALK/Smad signaling.ResultsWe found that the expression of Nodal was significantly increased in bladder cancer tissues and cell lines. Downregulation of Nodal effectively weakened cell proliferation, clone formation, and cell migration and invasion abilities. The protein expression levels of CDC6, E-cadherin, MMP-2, and MMP-9 were also altered by downregulation of Nodal. Knockdown of Nodal also blocked the expression of ALK4, ALK7, Smad2, and Smad4, which are involved in ALK/Smad signaling. Additionally, the ALK4/7 receptor blocker SB431542 reversed the promotive effects of Nodal overexpression on bladder cancer cell proliferation, migration, and invasion.ConclusionOur study indicated that Nodal functions as an oncogene by regulating cell proliferation, migration, and invasion in bladder cancer via the ALK/Smad signaling pathway, thereby providing novel insights into its role in bladder cancer treatment.

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MicroRNA-148b suppresses proliferation, migration, and invasion of nasopharyngeal carcinoma cells by targeting metastasis-associated gene 2

Cited by 16 publications

References 25 publications

Dynamic Changes in Plasma MicroRNAs Have Potential Predictive Values in Monitoring Recurrence and Metastasis of Nasopharyngeal Carcinoma

Dynamic Changes in Plasma MicroRNAs Have Potential Predictive Values in Monitoring Recurrence and Metastasis of Nasopharyngeal Carcinoma

miR-184 Inhibits Tumor Invasion, Migration and Metastasis in Nasopharyngeal Carcinoma by Targeting Notch2

Nodal regulates bladder cancer cell migration and invasion via the ALK/Smad signaling pathway

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