Expression profiles and prognostic value of miRNAs in retinoblastoma

Delsin, Lara Elis Alberici; Salomão, Karina Bezerra; Pezuk, Julia Alejandra; Brassesco, María Sol

doi:10.1007/s00432-018-2773-7

Cited by 32 publications

(26 citation statements)

References 106 publications

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“…Dysregulation of miRNAs has been shown to be closely correlated with the malignant development of RB. [17][18][19] Multiple miRNAs have been implicated in the aggressive behavior of RB by acting as tumor suppressors or oncogenes. [33][34][35] Accordingly, further investigation of the specific miRNAs related to the development and progression of RB might facilitate the identification of promising therapeutic strategies for patients with RB.…”

Section: Discussionmentioning

confidence: 99%

“…[14][15][16] Numerous studies have shown that the expression profiles of various miRNAs are altered in RB. [17][18][19] For example, miR-101-3p, 20 miR-506-3p, 21 and miR-874 22 are expressed at low levels in RB and function as tumor-suppressive miRNAs. In contrast, miR-10b, 23 miR-198, 24 and miR-498 25 are upregulated in RB and have a tumor-promoting functions.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway

Wang

et al. 2019

CMAR

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Purpose: Previous studies have revealed that microRNA-665 (miR-665) is dysregulated in a variety of human cancers. However, little is known regarding its expression profiles and functions in retinoblastoma (RB). Therefore, the aims of our study were to evaluate miR-665 expression in RB and determine the precise roles of miR-665 in the progression of RB. Patients and methods: Herein, RT-qPCR was used to determine miR-665 expression levels in RB tissues and cell lines, and a series of functional experiments were performed to explore the influence of miR-665 on RB cell proliferation, colony formation, apoptosis, migration, and invasion as well as tumor growth. The molecular mechanisms underlying the tumor-suppressive action of miR-665 in RB were also explored. Results: We found that miR-665 was markedly reduced in RB tissues and cell lines and that lower miR-665 expression was strongly associated with tumor size, TNM stage, and differentiation in patients with RB. Exogenous expression of miR-665 suppressed cell proliferation, colony formation, migration, and invasion, and induced cell apoptosis in RB cells, while silencing miR-665 expression had the opposite effects. In addition, upregulation of miR-665 decreased the tumor growth of RB cells in vivo. High-mobility group box 1 (HMGB1) was identified as a direct target of miR-665 in RB cells, and decreasing the expression of HMGB1 simulated the regulatory effects of miR-665 overexpression in RB cells, while knockdown of HMGB1 expression counteracted the miR-665-mediated antitumor effects in RB cells. Moreover, miR-665 was shown to regulate the Wnt/β-catenin signaling pathway by targeting HMGB1 in vitro and in vivo. Conclusion: Taken together, our in vitro and in vivo results suggest that miR-665 acts as a tumor-suppressive miRNA in RB by directly targeting HMGB1 and inactivating the Wnt/βcatenin pathway. Hence, this miRNA is a candidate prognostic biomarker and therapeutic target in patients with RB.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway

Wang

et al. 2019

CMAR

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“…In total, 4,469 genes of miRNAs, including 1,881 precursor and 2,588 mature miRNAs, have been identified in the human genome, according to miRBase. In the field of RB research, a variety of different miRNAs have been revealed to be aberrantly expressed, and their anomalous expression plays important roles in the regulation of multiple cancer-related processes, including cell survival, proliferation, apoptosis, metastasis, angiogenesis and epithelial-mesenchymal transition (10). For instance, miR-98 (11), miR-186 (12) and miR-665 (13) are weakly expressed in RB and restrain tumor progression; on the contrary, miR-93 (14), miR-106b (15) and miR-198 are overexpressed in RB and promote tumor aggressiveness.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

Shi³

et al. 2020

Oncol Rep

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MicroRNA-936 (miR-936) has been reported to play important roles in the progression of non-small cell lung cancer and glioma. However, the expression and functions of miR-936 in retinoblastoma (RB) remain elusive and need to be further elucidated. Herein, the aims were to measure miR-936 expression in RB, identify the functional importance of miR-936 in the oncogenicity of RB, and investigate the underlying molecular mechanisms. Reverse-transcription quantitative PCR was carried out to determine miR-936 expression in RB tissues and cell lines. Cell proliferation, colony formation, apoptosis, migration, and invasion in vitro and tumor growth in vivo were examined respectively by Cell Counting Kit-8, colony formation, flow cytometric, and Transwell migration and invasion assays and a subcutaneous heterotopic xenograft experiment. The potential target of miR-936 was predicted by bioinformatic analysis and was subsequently validated by luciferase reporter assay, reverse-transcription quantitative PCR, and western blotting. miR-936 expression was weak in both RB tissues and cell lines and was correlated with differentiation, lymph node metastasis and TNM staging in RB. RB cell proliferation, colony formation, migration, and invasion in vitro and tumor growth in vivo were attenuated by exogenous miR-936, whereas apoptosis was enhanced by miR-936 overexpression. Further molecular investigation identified histone deacetylase 9 (HDAC9) as a direct target gene of miR-936 in RB cells. HDAC9 depletion had effects similar to those of miR-936 overexpression in RB cells. Recovery of HDAC9 expression counteracted the tumor-suppressive action of miR-936 on the oncogenicity of RB cells. Ectopic miR-936 expression deactivated the PI3K/AKT pathway in RB cells in vitro and in vivo by decreasing HDAC9 expression. Downregulated miR-936 is related to poor prognosis in RB, and its upregulation inhibits RB aggressiveness via direct targeting of HDAC9 mRNA and thereby inactivation of the PI3K/AKT pathway.

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“…miRNAs act as gene expression regulators by imperfect or near-perfect base pairing with the 3′-UTRs of their target mRNAs, thereby resulting in translation suppression and/or mRNA degradation 12. Multiple lines of evidence have demonstrated that nearly all cellular physiological and pathological processes are closely regulated by miRNAs including carcinogenesis and cancer progression 13–15. The aberrant expression of miRNAs is a common and important feature of breast cancer, and their dysregulation participates in the malignant phenotypes of breast cancer by acting as oncogenes or tumor suppressors 16–18.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-876 is sponged by long noncoding RNA LINC00707 and directly targets metadherin to inhibit breast cancer malignancy

Liu

Sun

2019

CMAR

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Background: MicroRNA-876-5p (miR-876) dysregulation contributes to the aggressiveness of various types of human cancer. This study was aimed at measuring miR-876 expression in breast cancer, determining the specific roles of miR-876 in the progression of breast cancer and understanding the corresponding molecular mechanisms. Materials and methods: miR-876 expression in breast cancer tissues and cell lines was quantified via RT-qPCR. The effect of miR-876 upregulation on the malignant phenotype of breast cancer cells was investigated using CCK-8 assays, flow cytometry, Transwell migration and invasion assays and tumor xenograft experiments. The mechanisms underlying the tumor-suppressive action of miR-876 in breast cancer cells were explored using bioinformatic analysis, luciferase reporter assays, RT-qPCR and Western blot analysis. Results: miR-876 was found to be underexpressed in breast cancer tissues and cell lines. Decreased miR-876 expression notably correlated with lymphatic invasion metastasis, TNM stage and differentiation grade. Overall survival was lower among patients with breast cancer and low miR-876 expression than in patients with high miR-876 expression. Restoration of miR-876 expression decreased breast cancer cell proliferation, migration and invasion in vitro and restricted tumor growth in vivo as well as increased cell apoptosis. Metadherin (MTDH) was identified as a novel target of miR-876 in breast cancer cells. Furthermore, long intergenic nonprotein-coding RNA 707 (LINC00707) acted as a molecular sponge for miR-876, thereby regulating MTDH expression in breast cancer. Finally, silencing miR-876 expression attenuated the influence of a LINC00707 knockdown on the malignancy of breast cancer cells. Conclusion: This study, thus, revealed the vital functions of the LINC00707-miR-876-MTDH pathway in breast cancer and provided attractive targets and markers for its treatment.

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Expression profiles and prognostic value of miRNAs in retinoblastoma

Cited by 32 publications

References 106 publications

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

<p>MicroRNA-876 is sponged by long noncoding RNA LINC00707 and directly targets metadherin to inhibit breast cancer malignancy</p>

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Expression profiles and prognostic value of miRNAs in retinoblastoma

Cited by 32 publications

References 106 publications

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/&beta;-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/&beta;-catenin pathway</p>

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

<p>MicroRNA-876 is sponged by long noncoding RNA LINC00707 and directly targets metadherin to inhibit breast cancer malignancy</p>

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<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>