MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Yang, Hongwei; Huang, Yuesheng; He, Jianlin; Chai, Guangrui; Di, Yu; Wang, Aiyuan; Gui, Dongmei

doi:10.1042/bsr20200392

Cited by 21 publications

(15 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous researches have reported that miRNAs are powerful modulators of complex biological processes, including cell growth, apoptosis, metastasis, and metabolism [ 25 ], Additionally, it was also revealed that aberrant miRNA expression was associated with the progression of many types of cancer [ 26 , 27 ], including OSCC [ 28 ]. miR-486-3p and miR-637 are well-recognized tumor suppressors [ 29 , 30 ] and have been uncovered to impede OSCC tumorigenesis [ 15 , 16 ]. In this study, a decreased miR-486-3p or miR-637 expression was observed in OSCC.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Circ_0005320 promotes oral squamous cell carcinoma tumorigenesis by sponging microRNA-486-3p and microRNA-637

Zheng

Gong

et al. 2021

Bioengineered

View full text Add to dashboard Cite

Circ_0005320 was found to be elevated in oral squamous cell carcinoma (OSCC) and accelerated OSCC progression. Here, the potential mechanism of circ_0005320 in OSCC tumorigenesis was explored. The quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to detect the expression of circ_0005320, miR-486-3p, and miR-637. In vitro assays were conducted using cell counting kit-8, colony formation, transwell, angiogenesis, and flow cytometry assays. The targeting relationship between microRNA (miR)-486-3p and miR-637 or circ_0005320 was confirmed using the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) pathway-related proteins were analyzed using Western blot. The murine xenograft model was established to perform in vivo assay. Circ_0005320 expression was higher in OSCC tissues and cells. Knockdown of circ_0005320 suppressed OSCC cell growth, migration, invasion, and induced cell apoptosis in vitro, as well as impeded tumor growth in vivo. Mechanistically, miR-486-3p or miR-637 were confirmed to be a target of circ_0005320. Moreover, the inhibitory effects of circ_0005320 silencing on OSCC growth were reversed by the inhibition of miR-486-3p or miR-637. We also found that circ_0005320-miR-486-3p/miR-637 axis mediated the activation of JAK2/STAT3 pathway. This study revealed a novel regulatory network of circ_0005320-miR-486-3p/miR-637 axis in OSCC progression, suggesting that circ_0005320 might be a potential biomarker and therapeutic target for OSCC.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Circ_0005320 promotes oral squamous cell carcinoma tumorigenesis by sponging microRNA-486-3p and microRNA-637

Zheng

Gong

et al. 2021

Bioengineered

View full text Add to dashboard Cite

show abstract

“…ECM1 has been proved to play an essential role in embryonic chondrogenesis ( Deckers et al, 2001 ), skin differentiation ( Mcgrath, 2015 ), epithelial cell proliferation ( Yang et al, 2020 ), Angiogenesis ( Wang B et al, 2020 ), tumorigenesis ( Wang et al, 2003 ) and other biological processes. Emerging evidence has revealed that ECM1 is upregulated in many cancers and contributes to a worse patient prognosis ( Lee et al, 2015 ; Chen et al, 2016 ; Gan et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

ECM1 regulates the resistance of colorectal cancer to 5-FU treatment by modulating apoptotic cell death and epithelial-mesenchymal transition induction

et al. 2022

View full text Add to dashboard Cite

5-Fluorouracil (5-FU) chemoresistance is a persistent impediment to the efficient treatment of many types of cancer, yet the molecular mechanisms underlying such resistance remain incompletely understood. Here we found CRC patients resistant to 5-FU treatment exhibited increased extracellular matrix protein 1 (ECM1) expression compared to CRC patients sensitive to this chemotherapeutic agent, and higher levels of ECM1 expression were correlated significantly with shorter overall survival and disease-free survival. 5-FU resistant HCT15 (HCT15/FU) cells expressed significantly higher levels of ECM1 relative to parental HCT15 cells. Changes in ECM1 expression altered the ability of both parental and HCT15/FU cells to tolerate the medication in vitro and in vivo via processes associated with apoptosis and EMT induction. From a mechanistic perspective, knocking down and overexpressing ECM1 in HCT15/FU and HCT15 cell lines inhibited and activated PI3K/AKT/GSK3β signaling, respectively. Accordingly, 5-FU-induced apoptotic activity and EMT phenotype changes were affected by treatment with PI3K/AKT agonists and inhibitors. Together, these data support a model wherein ECM1 regulates CRC resistance to 5-FU via PI3K/AKT/GSK3β pathway-mediated modulation of apoptotic resistance and EMT induction, highlighting ECM1 as a promising target for therapeutic intervention for efforts aimed at overcoming chemoresistance in CRC patients.

show abstract

“…Various studies have established hsa-miR-486 to be a tumor suppressor [55]. In many cancers including OSCC, its downregulation is associated with migration and invasion [41].…”

Section: Discussionmentioning

confidence: 99%

Discovery of new deregulated miRNAs in gingivo buccal carcinoma using Group Benjamini Hochberg method: a commentary on “A quest for miRNA bio-marker: a track back approach from gingivo buccal cancer to two different types of precancers”

Koner

Sarkar

Laha

2023

Preprint

View full text Add to dashboard Cite

This formal comment is in response to 'A quest for miRNA bio-marker: a track back approach from gingivo buccal cancer to two different types of precancers' written by De Sarkar and colleagues in 2014. The above-mentioned paper found seven miRNAs to be significantly deregulated in 18 gingivo-buccal cancer samples. However, they suspected more miRNAs to be deregulated based on their exploratory statistical analysis. To control the false discovery rate (FDR), the authors used the Benjamini Hochberg (BH) method, which does not leverage any available biological information on the miRNAs. In this work, we show that some specialized versions of the BH method, which can exploit positional information on the miRNAs, can lead to seven more discoveries with this data. Specifically, we group the closely located miRNAs, and use the group Benjamini Hochberg (GBH) methods (Hu et al., 2010), which reportedly have more statistical power than the BH method (Liu et al., 2019). The whole transcriptome analysis of Sing et al. (2017) and previous literature on the miRNAs suggest that most of the newly discovered miRNAs play a role in oncogenesis. In particular, the newly discovered miRNAs include hsa-miR-1 and hsa-miR-21-5p, whose cancer-related activities are well-established. Our findings indicate that incorporating the GBH method into suitable microarray studies may potentially enhance scientific discoveries via the exploitation of additional biological information.

show abstract

MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Cited by 21 publications

References 46 publications

RETRACTED ARTICLE: Circ_0005320 promotes oral squamous cell carcinoma tumorigenesis by sponging microRNA-486-3p and microRNA-637

RETRACTED ARTICLE: Circ_0005320 promotes oral squamous cell carcinoma tumorigenesis by sponging microRNA-486-3p and microRNA-637

ECM1 regulates the resistance of colorectal cancer to 5-FU treatment by modulating apoptotic cell death and epithelial-mesenchymal transition induction

Discovery of new deregulated miRNAs in gingivo buccal carcinoma using Group Benjamini Hochberg method: a commentary on “A quest for miRNA bio-marker: a track back approach from gingivo buccal cancer to two different types of precancers”

Contact Info

Product

Resources

About