MicroRNA-449a Inhibits Tumor Metastasis through AKT/ERK1/2 Inactivation by Targeting Steroid Receptor Coactivator (SRC) in Endometrial Cancer

Hu, Yuan; Wu, Anyue; Xu, Cong; Song, Keqi; Wang, Wenjing; Yin, Xiang; Di, Wen; Hong, Zubei; Qiu, Lihua

doi:10.7150/jca.27748

Cited by 17 publications

(16 citation statements)

References 23 publications

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“…In the mechanistic studies, we further demonstrated that EVI1 would regulate NPC cell migration and tumor sphere formation via miR-449a. This observation further supports the previous findings that miR-449a can function as a tumor suppressor to inhibit tumor cell migration, invasion and proliferation in other tumor cell types [39][40][41]50,51]. Apart from the regulation of miR-449a expression, previous global pathway analysis showed that EVI1 could bind to 78% of genes involved in the regulation of the Jak-Stat signaling [52].…”

Section: Discussionsupporting

confidence: 90%

“…Although the mechanism of miR-449a-mediated inhibition was not further examined in the present study, Li and co-workers had previously demonstrated that miR-449a could regulate glycolysis and inhibit the growth of NPC cells by targeting lactate dehydrogenase A (LDHA) [38]. Apart from LDHA, miR-449a had also been shown to inhibit the growth of endometrial cancer, osteosarcoma, breast cancer, glioma and non-small-cell lung cancer cells by targeting the steroid receptor coactivator [39], Enhancer Of Zeste 2 Polycomb Repressive Complex 2 (EZH2) [40], Pleomorphic adenoma gene like-2 [41], Notch Receptor 1 (Notch1) [42] and High Mobility Group Box 1 (HMGB1) [43], respectively. In NPC, EZH2 has been shown to be overexpressed in biopsy samples [44] and has been functionally implicated in the control of cell growth and cell migration [45,46].…”

Section: Discussionmentioning

confidence: 82%

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Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation

Chan

Lung

Ngan

et al. 2020

IJMS

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The Wnt signaling pathway is one of the major signaling pathways used by cancer stem cells (CSC). Ecotropic Viral Integration Site 1 (EVI1) has recently been shown to regulate oncogenic development of tumor cells by interacting with multiple signaling pathways, including the Wnt signaling. In the present study, we found that the Wnt modulator ICG-001 could inhibit the expression of EVI1 in nasopharyngeal carcinoma (NPC) cells. Results from loss-of-function and gain-of-function studies revealed that EVI1 expression positively regulated both NPC cell migration and growth of CSC-enriched tumor spheres. Subsequent studies indicated ICG-001 inhibited EVI1 expression via upregulated expression of miR-96. Results from EVI1 3′UTR luciferase reporter assay confirmed that EVI1 is a direct target of miR-96. Further mechanistic studies revealed that ICG-001, overexpression of miR-96, or knockdown of EVI1 expression could restore the expression of miR-449a. The suppressive effect of miR-449a on the cell migration and tumor sphere formation was confirmed in NPC cells. Taken together, the miR-96/EVI1/miR-449a axis is a novel pathway involved in ICG-001-mediated inhibition of NPC cell migration and growth of the tumor spheres.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 82%

Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation

Chan

Lung

Ngan

et al. 2020

IJMS

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“…17 Interestingly, miR-449a has been also disclosed to function as a suppressor in the development of EC. 18,19 Up-regulation of miR-449a inhibits the proliferation, migration and invasion of EC cells, thus eventually retarding the growth of EC. 20 Nevertheless, we are still unclear whether the suppressive effects of miR-449a on EC progression is regulated by LINC01106.…”

Section: Introductionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Gao¹,

Yu²,

Zhang³

et al. 2020

OTT

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Endometrial cancer (EC) is an aggressive tumor in females and the development of EC is considered to regulate by some long non-coding RNAs (lncRNAs). Therefore, this study aimed to investigate the regulatory mechanism of lncRNA LINC01106 on EC. Methods: The expression of lncRNA LINC01106, miR-449a and MET in EC tissues and cells was detected by qRT-PCR. Through MTT, wound healing and transwell invasion assays, the proliferation, migration and invasion of EC cells were detected, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibiting effect of LINC01106 knockdown on EC in vivo. The interactions between miR-449a and LINC01106/ MET were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein level of MET. Results: LncRNA LINC01106 expression was highly up-regulated in EC tissues and cells. The proliferation, migration and invasion of EC cells in vitro were inhibited by the transfection of sh-LINC01106. The growth of tumor xenograft was suppressed by injection of sh-LINC01106. MiR-449a was a target of LINC01106and was negatively modulated by LINC01106. MiR-449a overexpression suppressed the proliferation, migration and invasion of EC cells. In addition, MET was identified as a target gene of miR-449a. Both the high expression of miR-449a and low expression of MET reversed the inhibiting effects of LINC01106 knockdown on Ishikawa cells. Conclusion: Silencing of LINC01106 inhibits the occurrence and development of EC via regulating the miR-449a/MET axis. This study provides a possible therapeutic strategy for EC.

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“…This systematic review identified 105 original articles and two literature reviews reporting the expression pattern of miRNAs [ 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 ,…”

Section: Resultsmentioning

confidence: 99%

MicroRNA as Epigenetic Modifiers in Endometrial Cancer: A Systematic Review

Favier

Rocher

Larsen

et al. 2021

Cancers

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The objective of this systematic review is to summarize our current knowledge on the influence of miRNAs in the epigenetic deregulation of tumor-related genes in endometrial cancer (EC). We conducted a literature search on the role of miRNAs in the epigenetic regulation of EC applying the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The following terms were used: microRNA, miRNA, miR, endometrial cancer, endometrium, epigenetic, epimutation, hypermethylation, lynch, deacetylase, DICER, novel biomarker, histone, chromatin. The miRNAs were classified and are presented according to their function (tumor suppressor or onco-miRNA), their targets (when known), their expression levels in EC tissue vs the normal surrounding tissue, and the degree of DNA methylation in miRNA loci and CpG sites. Data were collected from 201 articles, including 190 original articles, published between November 1, 2008 and September 30, 2020 identifying 313 different miRNAs implicated in epigenetic regulation of EC. Overall, we identified a total of 148 miRNAs with decreased expression in EC, 140 miRNAs with increased expression in EC, and 22 miRNAs with discordant expression levels. The literature implicated different epigenetic phenomena including altered miRNA expression levels (miR-182, -230), changes in the methylation of miRNA loci (miR-34b, -129-2, -130a/b, -152, -200b, -625) and increased/decreased methylation of target genes (miR-30d,-191). This work provides an overview of all miRNAs reported to be involved in epigenetic regulation in EC including DNA methylation and RNA-associated silencing. These findings may contribute to novel strategies in diagnosis, risk assessment, and treatments aimed at miRNAs, their target genes or DNA methylation.

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MicroRNA-449a Inhibits Tumor Metastasis through AKT/ERK1/2 Inactivation by Targeting Steroid Receptor Coactivator (SRC) in Endometrial Cancer

Cited by 17 publications

References 23 publications

Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation

Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

MicroRNA as Epigenetic Modifiers in Endometrial Cancer: A Systematic Review

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