MIR-300 in the imprinted DLK1-DIO3 domain suppresses the migration of bladder cancer by regulating the SP1/MMP9 pathway

Yan, Huaqing; Li, Jiangfeng; Ying, Yufan; Xie, Haiyun; Chen, Hong; Xu, Xin; Zheng, Xiangyi

doi:10.1080/15384101.2018.1557490

Cited by 28 publications

(16 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MMP9 is one of key member of MMPs family. Elevating MMP9 expression plays a key role in the progression of many tumors, such as bladder cancer [25], esophageal squamous cell carcinoma [26], and intrahepatic cholangiocarcinoma [27]. Our study proved that M2 macrophages can increase HCC cells invasion and migration by upregulating MMP9 expression, this conclusion was strengthened by the outcome in response to the MMP9-shRNA which could block the biochemical and cell behavior induced by M2 macrophages in the HCC tumor microenvironment.…”

Section: Discussionsupporting

confidence: 52%

M2 Macrophages Promote HCC Cells Invasion and Migration via miR-149-5p/MMP9 Signaling

Liu¹,

Yin²,

Ouyang³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

The roles of M2 macrophages on promoting tumor progression and chemotherapy resistance have been well studied in many cancers, such as pancreatic cancer, kidney cancer and so on, but its linkage to HCC cells still remains unclear. Here we found that M2 macrophages could alter miR-149-5p to increase MMP9 expression in HCC cells and mechanism dissection revealed that miR-149-5p might directly target the 3'UTR of MMP9-mRNA to suppress its translation. The in vivo orthotopic xenografts mouse model with oemiR-149-5p also validated in vitro data. Together, these findings suggest that M2 macrophages may through altering the miR-149-5p to promote HCC progression and targeting the M2 macrophages/ miR149-5P/MMP9 signaling may help in the development of the novel therapies to better suppress the HCC progression.

show abstract

Section: Discussionsupporting

confidence: 52%

M2 Macrophages Promote HCC Cells Invasion and Migration via miR-149-5p/MMP9 Signaling

Liu¹,

Yin²,

Ouyang³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

show abstract

“…MMP-9 is one key member of the MMPs family. The progression of various types of cancer, such as bladder, breast, esophageal squamous cell carcinoma, intrahepatic cholangiocarcinoma, hepatocellular carcinoma, is driven by the up-regulation of MMP-9 [ 135 , 136 , 137 , 138 , 139 ]. MMP-9 is able to cleave extracellular matrix components such as collagen or fibronectin, as well as many other non-collagenous substrates.…”

Section: Myc–a Key Player In the Tumor Microenvironment (Tme)mentioning

confidence: 99%

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Meškytė

Keskas

Ciribilli

2020

IJMS

View full text Add to dashboard Cite

The Myc family of oncogenes is deregulated in many types of cancer, and their over-expression is often correlated with poor prognosis. The Myc family members are transcription factors that can coordinate the expression of thousands of genes. Among them, c-Myc (MYC) is the gene most strongly associated with cancer, and it is the focus of this review. It regulates the expression of genes involved in cell proliferation, growth, differentiation, self-renewal, survival, metabolism, protein synthesis, and apoptosis. More recently, novel studies have shown that MYC plays a role not only in tumor initiation and growth but also has a broader spectrum of functions in tumor progression. MYC contributes to angiogenesis, immune evasion, invasion, and migration, which all lead to distant metastasis. Moreover, MYC is able to promote tumor growth and aggressiveness by recruiting stromal and tumor-infiltrating cells. In this review, we will dissect all of these novel functions and their involvement in the crosstalk between tumor and host, which have demonstrated that MYC is undoubtedly the master regulator of the tumor microenvironment. In sum, a better understanding of MYC’s role in the tumor microenvironment and metastasis development is crucial in proposing novel and effective cancer treatment strategies.

show abstract

“…What's more, further luciferase reporter assay con rmed such regulatory relation. MMP9 is a well-kown tumor promotor and mainly enhances the invasion and metastasis of various tumors [27][28][29]. Moreover, MMP9 also participates in regulating tumor growth [30].…”

Section: Discussionmentioning

confidence: 99%

Mir-483-3p, Mediated by KLF9, Functions as Tumor Suppressor in Testicular Seminoma via Targeting MMP9

Zhang

Ruan

Gao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Seminoma (SEM) is the most frequent testicular germ cell tumor with a high incidence in young men. The present study aims to explore the function and regulatory mechanism of miR-483-3p in SEM.Methods: RT-qPCR was performed to investigate miR-483-3p levels in SEM tissues. The effect of miR-483-3p on TCam-2 cells was assessed by CCK-8, colony formation, cell migration and invasion assays. Luciferase reporter assays were performed to investigate the interaction between miR-483-3p and MMP9 and then the recovery experiments were performed. Moreover, the potential upstream regulator of miR-483-3p was predicted based on JASPAR database.Results: miR-483-3p was down‐regulated in SEM tissues versus paracancerous normal tissues. The expression level of miR-483-3p was significantly associated with tumor stage by RT-qPCR. Functionally, miR-483-3p over-expression suppressed cell growth, migration and invasion in SEM cell lines. Mechanically, miR-483-3p negatively regulated MMP9 by directly binding to its 3’-UTR. The over-expression of miR-483-3p could reverse the promoting role of MMP9 over-expression on the proliferation, migration and invasion of TCam-2 cells. Moreover, KLF9 was identified as a potential upstream regulator of miR-483-3p and functions as a tumor suppressor.Conclusions: In general, our study suggested that miR-483-3p could inhibit the cell growth, migration and invasion of testicular SEM by targeting MMP9. Moreover, KLF9 is an upstream positive regulator of miR-483-3p and also functions as a tumor suppressor in SEM.

show abstract

MIR-300 in the imprinted DLK1-DIO3 domain suppresses the migration of bladder cancer by regulating the SP1/MMP9 pathway

Cited by 28 publications

References 43 publications

M2 Macrophages Promote HCC Cells Invasion and Migration via miR-149-5p/MMP9 Signaling

M2 Macrophages Promote HCC Cells Invasion and Migration via miR-149-5p/MMP9 Signaling

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Mir-483-3p, Mediated by KLF9, Functions as Tumor Suppressor in Testicular Seminoma via Targeting MMP9

Contact Info

Product

Resources

About