miR-34a, miR-424 and miR-513 inhibit MMSET expression to repress endometrial cancer cell invasion and sphere formation

Dong, Peixin; Xiong, Ying; Yue, Junming; Hanley, Sharon J.B.; Watari, Hidemichi

doi:10.18632/oncotarget.25298

Cited by 39 publications

(41 citation statements)

References 28 publications

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“…4 Among them, non-coding RNAs, which contain microRNA (miRNA) and long noncoding RNA (lncRNA), were shown to be dysregulated in OC and have been recognized as new targets of treatments in many tumors. 5,6 In cancer cells, miRNAs regulate the gene expression post-transcriptionally by binding to mRNA 3′-untranslated region (3′-UTR), leading to translational repression or mRNA degradation. 7 Recent studies have demonstrated that lncRNA EMX2OS was significantly upregulated in gastric cancer tissues compared to the matched control tissues.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA EMX2OS Induces Proliferation, Invasion and Sphere Formation of Ovarian Cancer Cells via Regulating the miR-654-3p/AKT3/PD-L1 Axis</p>

Duan¹,

Fang²,

Wang³

et al. 2020

CMAR

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Long noncoding RNA (lncRNA) deregulation is frequent in human ovarian cancers (OCs), but the role of specific miRNAs involved in this disease remains elusive. LncRNA EMX2OS was previously reported to act as an oncogene in human cancers. However, their accurate expression, function and underlying mechanisms in OC are largely unclear. Materials and Methods: The levels of EMX2OS in OC tissues and cell lines were determined by quantitative real-time PCR, and the function of EMX2OS was then analyzed both in vitro and in vivo. Luciferase assays and immunoprecipitation assays were performed to analyze the association between EMX2OS and miR-654 expression in OC cells. Results: EMX2OS is overexpressed in human ovarian cancer tissues. Knockdown of EMX2OS reduced, while overexpression of EMX2OS enhanced the proliferation, invasion and sphere formation of OC cells. In addition, EMX2OS enhanced tumor growth in an in vivo xenograft model of human OC. We discovered that EMX2OS directly binds to miR-654 and suppresses its expression, thus leading to the upregulation of AKT3, which served as a direct target of miR-654. Moreover, miR-654 inhibited cell proliferation, invasion and sphere formation, and restoration of AKT3 reversed the effects of EMX2OS silencing or miR-654 overexpression. Furthermore, PD-L1 was identified as the key oncogenic component acting downstream of AKT3 in OC cells. Ectopic expression of PD-L1 reversed the anti-cancer functions by EMX2OS knockdown, AKT3 silencing or miR-654 upregulation in OC cells. Conclusion: These results demonstrated that the EMX2OS/miR-654/AKT3/PD-L1 axis confers aggressiveness in ovarian cancer and may represent a therapeutic target for OC metastasis.

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Section: Introductionmentioning

confidence: 99%

<p>LncRNA EMX2OS Induces Proliferation, Invasion and Sphere Formation of Ovarian Cancer Cells via Regulating the miR-654-3p/AKT3/PD-L1 Axis</p>

Duan¹,

Fang²,

Wang³

et al. 2020

CMAR

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“…In human tumors, aberrant expression of lncRNAs is associated with tumorigenesis, metastasis and chemotherapy resistance (Balas and Johnson, 2018;Dong et al, 2019). In addition, microRNAs (miRNAs) are small endogenous non-coding RNAs composed of approximately 19-24 nucleotides that regulate target genes posttranscriptionally (Dong et al, 2017), and miRNAs play key roles in the modulation of tumor growth and metastasis (Dong et al, 2017(Dong et al, , 2018b. It has been reported that miR-3127 acts as either a tumor suppressor or an oncogene in cancers, such as glioma (Pan et al, 2019), lung cancer (Sun et al, 2014;Yang et al, 2018) and hepatocellular carcinoma (Jiang et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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Recent studies suggested that microRNA-3127 (miR-3127) was dysregulated in multiple tumor types and has important roles in tumorigenesis and cancer progression. However, its biological roles and the mechanisms that regulate its expression in bladder cancer (BCA) remain to be determined. The expression level of miR-3127 was measured in BCA tissues and its cellular functions were examined using both in vitro and in vivo experiments. The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines. Lower miR-3127 levels were associated with worse survival in BCA patients. The overexpression of miR-3127 impaired BCA cell proliferation and invasion, and the knockdown of miR-3127 enhanced BCA cell proliferation and invasion in vitro. Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.

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“…Furthermore, the low expression of miR-513 was coupled with PD-L1 overexpression in retinoblastoma [26]. Recent studies showed that miR-513 hinders cell invasion and metastasis in endometrial cancer and that it is implicated in gemcitabine resistance in bladder cancer [27,28]. These findings support the potential utility of miR-513 mimics to target these cancer types.…”

Section: Mirnas Direct Regulation Of Pd-l1 Expressionmentioning

confidence: 62%

“…Therefore, the use of miR-138-5p mimics is anticipated to be important in modulating the antitumor immunity in both RCC and lung cancer. Recent studies showed that miR-513 hinders cell invasion and metastasis in endometrial cancer and that it is implicated in gemcitabine resistance in bladder cancer [27,28]. This miRNA inhibits the expression of PD-L1, in addition to hindering interferon gamma (IFN-c)-mediated PD-L1 expression in the cholangiocytes.…”

Section: Mirnas Direct Regulation Of Pd-l1 Expressionmentioning

confidence: 99%

Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment

et al. 2019

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Cancer immunotherapy represents a promising new era in cancer management due to the relatively high safety margins and selectivity, compared to the classical cancer chemotherapeutic agents. However, there is an imperative need to overcome tumor resistance in order to improve clinical outcomes and maximize the benefits of cancer immunotherapy. The interaction between the programmed cell death‐1 (PD‐1) receptor and its ligand PD‐L1 is a vital immune checkpoint that is often adopted by cancer cells to undergo immune evasion. PD‐1/PD‐L1 signaling is regulated at multiple levels through the crosstalk with other immune targets or relevant signaling partners involved in the cancer progression. Among the significant epigenetic players that are implicated in modulating the immune system are microRNAs (miRNAs). A complex system of these noncoding RNAs regulates the gene expression at the post‐transcriptional level and plays a significant role in the modulation of both innate and the adaptive immune systems. The expression profile of immune‐modulatory miRNAs might be useful as a predictive biomarker for the response and clinical outcomes in cancer immunotherapy. Therefore, in the current review, we highlighted the role of miRNAs in cancer immune evasion through a critical discussion of their impact on key immune checkpoints as well as the role of miRNAs in cancer progression and resistance.

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miR-34a, miR-424 and miR-513 inhibit MMSET expression to repress endometrial cancer cell invasion and sphere formation

Cited by 39 publications

References 28 publications

<p>LncRNA EMX2OS Induces Proliferation, Invasion and Sphere Formation of Ovarian Cancer Cells via Regulating the miR-654-3p/AKT3/PD-L1 Axis</p>

<p>LncRNA EMX2OS Induces Proliferation, Invasion and Sphere Formation of Ovarian Cancer Cells via Regulating the miR-654-3p/AKT3/PD-L1 Axis</p>

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment

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