miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

Liu, Shu; Hu, Chunmei; Wang, Yingxue; Shi, Guang; Li, Yarong; H, Wu

doi:10.3892/or.2016.4999

Cited by 34 publications

(28 citation statements)

References 33 publications

(39 reference statements)

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“…Recently, a study showed that STAT3 expression was upregulated in RB tissues, and that knockdown of STAT3 inhibited cell proliferation in vitro, and suppressed tumor growth in vivo (28,29). A recently study revealed that STAT3 was regulated by miR-124 in RB (18). In this study, we found that miR-29a overexpression significantly inhibited STAT3 expression and expression of its downstream genes cyclin D1, Bcl-2 and MMP-9.…”

Section: Discussionsupporting

confidence: 48%

miR-29a inhibits human retinoblastoma progression by targeting STAT3

Liu

Zhang

et al. 2017

Oncol Rep

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Retinoblastoma (RB) is the most common malignancy that occurs during childhood. Growing evidence supports a crucial role for microRNAs (miRNAs) in regulating the initiation and progression of RB. Aberrant expression of microRNA‑29a (miR‑29a) has been found in many types of cancers, but not including RB. Therefore, the aims of the present study were to evaluate the regulatory role and underlying mechanism of miR‑29a in human RB. In the present study, we found that miR‑29a expression was significantly downregulated in RB tissues and cell lines. Overexpression of miR‑29a in RB cells significantly inhibited cell proliferation, migration, and invasion and promoted cell apoptosis in vitro. Additionally, signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR‑29a in RB cells. miR‑29a overexpression in RB cells not only inhibited STAT3 expression but also altered expression of its downstream genes, including, Bcl2, cyclin D1 and matrix metalloproteinase 2 (MMP‑2). STAT3 mRNA expression was upregulated in RB tissues and negatively correlated with miR‑29a expression. Reintroduction of STAT3 without 3'‑untranslated region (3'UTR) reversed the inhibitory effects of miR‑29a on cell proliferation, migration and invasion. In vivo study confirmed that overexpression of miR‑29a also inhibited tumor formation of RB in a nude mouse model by repressing STAT3. Collectively, these data suggest that miR‑29a exerts a tumor suppressor effect on RB by repressing STAT3, supporting the targeting of miR‑29a as a potentially effective therapeutic method for RB.

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Section: Discussionsupporting

confidence: 48%

miR-29a inhibits human retinoblastoma progression by targeting STAT3

Liu

Zhang

et al. 2017

Oncol Rep

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“…Numerous miRNAs contribute to RB initiation and progression by regulating cell proliferation, cell cycle distribution, apoptosis, migration, invasion and metastasis (31)(32)(33). Therefore, further investigation on the expression, roles and associated mechanisms of RB-related miRNAs may be beneficial to develop novel strategies for patients with this malignancy.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Liu

et al. 2018

Oncol Rep

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Retinoblastoma (RB) is the most common primary intraocular malignancy during infancy and childhood worldwide. Numerous microRNAs (miRNAs) contribute to RB initiation and progression through the regulation of cell proliferation, cycle, apoptosis, migration, invasion and metastasis. Therefore, further investigation concerning the expression, roles and associated mechanisms of RB‑related miRNAs may be beneficial to develop novel strategies for patients with this malignancy. Recently, miRNA‑448 (miR‑448) has been reported to be aberrantly expressed and to play an important role in several types of human cancer. However, the expression patterns and biological roles of miR‑448 in RB have not been studied. The aim of the present study was to detect the expression levels of miR‑448 and investigate its functions in RB and its associated molecular mechanisms. In the present study, miR‑448 was significantly downregulated in RB tissues and cell lines. Upregulation of miR‑448 decreased cell proliferation and invasion and increased apoptosis in RB cells. Additionally, ρ‑associated coiled‑coil containing protein kinase 1 (ROCK1) was validated as a novel direct target gene of miR‑448 in RB. ROCK1 was overexpressed in RB tissues and inversely correlated with miR‑448 expression. Furthermore, ROCK1 silencing induced effects on the proliferation, invasion and apoptosis of RB cells similar to those observed following miR‑448 overexpression. Moreover, restoration of miR‑448 expression markedly reversed the effects of miR‑448 overexpression on RB cells, further supporting the hypothesis that ROCK1 is a direct functional target of miR‑448 in RB. Importantly, miR‑448 targeted ROCK1 to inhibit the activation of the PI3K/AKT signalling pathway in RB. These results demonstrated that miR‑448 may serve as a tumour suppressor in RB by directly targeting ROCK1 and regulating the PI3K/AKT signalling pathway, thereby suggesting that miR‑448 may be an effective therapeutic target for treating this aggressive cancer.

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“…In the past decade, miRNAs have been widely demonstrated to serve essential functions in the initiation and progression of RB via regulating the expression of specific genes (23). For instance, Liu et al (24) reported that the proliferation, migration and invasion of human RB cells were significantly suppressed by miR-124 in a signal transducer and activator of transcription 3-dependent manner. Lei et al (25) reported that miR-101 was downregulated in RB tissues and suppressed tumor cell growth and proliferation by inhibiting the expression of enhancer of (26) demonstrated that miR-34a was downregulated in RB tissues and enhanced tumor cell chemosensitivity and promoted cell death by targeting high mobility group box 1 to suppress autophagy.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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Numerous repor ts have indicated that microRNA-93-5p (miR-93-5p) is involved in the development and progression of human cancer, including non-small cell lung, gastric and breast cancer; however, the role of miR-93-5p in retinoblastoma (RB) remains unknown. In the present study, it was reported that miR-93-5p expression levels were significantly upregulated in RB tissues compared with in normal tissues by reverse transcription-quantitative polymerase chain reaction. Furthermore, it was demonstrated via cell counting kit-8 and Transwell assays that knockdown of miR-93-5p significantly suppressed the proliferation, migration and invasion of RB cells, but promoted cellular apoptosis. Regarding the underlying mechanism, the present study reported that phosphatase and tensin homolog (PTEN) was a direct target of miR-93-5p in RB cells. Overexpression of miR-93-5p significantly inhibited the expression of PTEN; opposing results were observed when PTEN expression was downregulated. Furthermore, the present study revealed that PTEN expression levels were downregulated and were inversely correlated with that of miR-93-5p in RB tissues. Additionally, the present study demonstrated that knockdown of PTEN in miR-93-5p-depleted RB cells significantly reversed the effects of miR-93-5p on cell proliferation, migration and invasion; miR-93-5p knockdown was suggested to promote PTEN expression, consequently inhibiting the activation of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Collectively, the results of the present study demonstrated that miR-93-5p may serve a role as an oncogene by modulating the PTEN/PI3K/AKT signaling pathway in RB, indicating that miR-93-5p may be a potential therapeutic target for the treatment of RB.

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miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

Cited by 34 publications

References 33 publications

miR-29a inhibits human retinoblastoma progression by targeting STAT3

miR-29a inhibits human retinoblastoma progression by targeting STAT3

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

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

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