MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

Cao, Yongliang; Xia, Fei; Wang, Ping; Gao, Meng

doi:10.3892/mmr.2018.9573

Cited by 11 publications

(8 citation statements)

References 34 publications

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“…Furthermore, in the RB development, PTEN showed an inhibitory effect and it served as the target of multiple miRNAs. For instance, it was the directly target of miR-93, and miR-198 in promoting human RB progression, and the decreased PTEN expression was also found, which was consists with our findings ( 34 , 35 ). In the present study, it was shown that miR-494 targeted PTEN in regulating RB cell progression, and PTEN overexpression can reverse the effect of miR-494 upregulation in RB cells.…”

Section: Discussionsupporting

confidence: 91%

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

Liu

Wang

et al. 2020

Oncol Lett

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Increasing evidence has indicated that the dysregulation of microRNA (miRNA) occur in the pathogenesis of retinoblastoma (RB). Aim of the present study was to investigate the possible role of miR-494 (miR-494-3p) in RB. It was demonstrated that miR-494 expression was increased in RB tissue samples and cell lines. Also, it was prominently associated with clinicopathological features. Functional assays showed that RB cell proliferation, invasion and migration can be promoted by miR-494 overexpression. Besides, phosphatase and tensin homolog (PTEN) was verified as a possible target of miR-494 by a luciferase assay, western blot and qRT-PCR assay in RB. miR-494 and PTEN expression was negatively related in a correlation analysis on tumor tissues of 66 patients. In addition, PTEN was proved to reverse miR-494 effect on RB cell progression. Moreover, PI3K/AKT signaling pathway was validated to take part in RB progression. Taken together, the current study proposes that miR-494 might function as a tumor promoter and regulates RB progression through targeting PTEN.

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Section: Discussionsupporting

confidence: 91%

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

Liu

Wang

et al. 2020

Oncol Lett

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“…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. miR-936 has been reported to exert important effects on the progression of non-small cell lung cancer (16) and glioma (17).…”

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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“…Of note is the relatively large decrease in miR-93 whose overexpression diminishes PTEN activity and promotes carcinogenesis through dysregulation of the PI3K/AKT pathway. 24 In general, our data show that reducing PLCβ1 substantially decreases the total amount of cellular miRs. Reduction of total cellular miRs with PLCβ1 down-regulation is in line with the large increase in small RNAs seen when PLCβ1 is overexpressed in HEK293 cells.…”

Section: Live Cell Imaging Of Mir Processingmentioning

confidence: 53%

Stimulation of the Gαq/phospholipase Cβ1 signaling pathway returns differentiated cells to a stem‐like state

et al. 2020

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Phospholipase Cβ1 is activated by Gαq to generate calcium signals in response to hormones and neurotransmitters. Besides carrying out this plasma membrane function, PLCβ1 has a cytosolic population that helps to drive the differentiation of PC12 cells by inhibiting a nuclease that promotes RNA‐induced silencing (C3PO). Here, we show that down‐regulating PLCβ1 or reducing its cytosolic population by activating Gαq to localize it to the plasma membrane returns differentiated PC12 and SK‐N‐SH cells to an undifferentiated state. In this state, PC12 cells have a spherical morphology, resume proliferation, and express the stem cell transcription factors nanog and Oct4. Similar changes are seen when C3PO is down‐regulated. This return to a stem‐like state is accompanied by shifts in multiple miR populations. Surprisingly, de‐differentiation can be induced by extended stimulation of Gαq where cells return to a spherical morphology and levels of specific miRs return to their undifferentiated values. In complementary studies, we followed the real‐time hydrolysis of a fluorescent‐tagged miR in cells where PLCβ1 or C3PO were down‐regulated in PC12 cells and find substantial differences in miR processing in the undifferentiated and differentiated states. Taken together, our studies suggest that PLCβ1, through its ability to regulate C3PO and endogenous miR populations, mediates the differentiation of two types of cultured neuronal cells.

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MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

Cited by 11 publications

References 34 publications

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

miR‑494 promotes progression of retinoblastoma via PTEN through PI3K/AKT signaling pathway

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

Stimulation of the Gαq/phospholipase Cβ1 signaling pathway returns differentiated cells to a stem‐like state

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