miR-25 promotes glioma cell proliferation by targeting CDKN1C

Zhang, Jihong; Gong, Xuhai; Tian, Kaiyu; Chen, Dongkai; Sun, Jing; Wang, Guangzhi; Guo, Ming

doi:10.1016/j.biopha.2015.02.005

Cited by 39 publications

(30 citation statements)

References 38 publications

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“…CDKN1C has been identified as a tumor suppressor due to its diminished expression and functions of blocking biological signs of progress of breast cancer [38]. CDKN1C inhibition by miR-25 is also known to induce glioma cell proliferation and invasion [39]. In consent with these findings, our results showed that inhibition of CDKN1C by EZH2 leads to a significant increase in melanoma cell viability and a decrease in oxidative stress and apoptosis due to catalyzing the H3K27 trimethylation.…”

Section: Discussionsupporting

confidence: 78%

Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation

Yan

et al. 2020

Cancer Cell Int

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Background: The significance of long non-coding RNAs (lncRNAs) in mediating oxidative stress of cancers has been implicated recently. This study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression. Methods: The lncRNA GAS5 expression pattern was examined in melanoma tissues and cells. The correlation of lncRNA GAS5, EZH2, and CDKN1C with survival rate of melanoma patients was analyzed. In melanoma cell lines, lncRNA GAS5 expression was overexpressed or knocked down to clarify its effects on cell viability, apoptosis, and oxidative stress. The interaction between lncRNA GAS5 and EZH2 was examined by RIP and RNA pull-down assays followed by verification of the target relationship between EZH2 and CDKN1C. Results: High expression of EZH2 and poor expression of lncRNA GAS5 and CDKN1C was observed in melanoma tissues and found to be correlated with the reduction in survival expectancy of melanoma patients. Overexpression of lncRNA GAS5 or CDKN1C or EZH2 knockdown could inhibit cell viability but enhance melanoma cell apoptosis and oxidative stress. Importantly, lncRNA GAS5 attenuated EZH2 expression by recruiting E2F4 to the EZH2 promoter region and knockdown of EZH2 upregulated CDKN1C expression by inhibiting the H3K27me3. Conclusion: The evidence provided by our study highlighted the involvement of lncRNA GAS5 in the translational suppression of EZH2 as well as the upregulation of CDKN1C, resulting in the promotion of melanoma cell apoptosis and oxidative stress.

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Section: Discussionsupporting

confidence: 78%

Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation

Yan

et al. 2020

Cancer Cell Int

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“…Li et al (25) reported that miR-25-3p expression is enhanced in gastric cancer tumor tissue, and its increased expression is correlated with tumor node metastasis stage and lymph node metastasis. The upregulation of miR-25-3p has also been observed in hepatocellular carcinoma (26), glioblastoma (27), glioma (28), cervical cancer (29) and cholangiocarcinoma (30).…”

Section: Discussionmentioning

confidence: 96%

Upregulation of microRNA-25-3p inhibits proliferation, migration and invasion of osteosarcoma cells in vitro by directly targeting SOX4

Zhou

Yue

et al. 2017

Molecular Medicine Reports

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Osteosarcoma (OS) is among the most common primary tumors of bone tissue, and occurs primarily in children and young adults. Despite the development of novel therapeutic approaches, the prognosis of OS remains poor. MicroRNAs (miRNAs) are involved in the development and progression of various types of human cancer and may have potential as novel therapeutic targets for cancer treatment. The present study aimed to investigate the expression and biological functions of miRNA‑25‑3p in OS, and explore the molecular mechanisms underlying its actions. In the present study, miRNA‑25‑3p was detected in OS tissues and cell lines. The functional roles of miRNA‑25‑3p in OS cells were evaluated using a Cell Counting Kit 8 assay and cellular migration and invasion assays. The molecular mechanisms underlying the tumor‑suppressing roles of miRNA‑25‑3p in OS were explored using bioinformatics analysis, luciferase reporter assay, western blotting and the reverse transcription‑quantitative polymerase chain reaction. The expression of miRNA‑25‑3p was revealed to be downregulated in OS tissues and cell lines compared with non‑tumor bone tissues and normal osteoblasts, respectively. miRNA‑25‑3p overexpression was demonstrated to significantly suppress the proliferation, migration and invasion of OS cells in vitro. In addition, sex‑determining region‑related high mobility group box (SOX) 4 was identified as a direct target gene of miRNA‑25‑3p, and was further investigated. Similarly to miRNA‑25‑3p overexpression, SOX4 knockdown was demonstrated to suppress OS cell proliferation, migration and invasion. Furthermore, SOX4 expression was revealed to be significantly upregulated in OS tissues compared with in adjacent non‑tumor bone tissues, and Spearman's correlation analysis indicated a negative correlation between SOX4 mRNA and miRNA‑25‑3p expression levels in OS tissues. The present findings suggested that miRNA‑25‑3p may act as a tumor suppressor by targeting SOX4 expression in bone tissue. Therefore, miRNA‑25‑3p may have potential as a novel therapeutic target for the treatment of patients with OS.

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“…Of interest, miR-25-3p displays a significant decrease after Sevo treatment. Additionally, miR-25-3p is well known oncogenic miRNA in several types of human cancers, including HCC (22)(23)(24); therefore, it appears plausible that Sevo's observed anticancer effects might be exerted through miR-25-3p in HCC cells.…”

Section: Sevo Downregulates the Expression Of Mir-25-3p In Hepatocellmentioning

confidence: 99%

Sevoflurane inhibits the proliferation and invasion of hepatocellular carcinoma cells through regulating the PTEN/Akt/GSK‑3β/β‑catenin signaling pathway by downregulating miR‑25‑3p

Cao

Ding

et al. 2020

Int J Mol Med

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Sevoflurane (Sevo) is one of the most frequently used volatile anesthetic agents in surgical oncology and has various effects on tumors, including inhibiting tumor growth, recurrence, and metastases; however, the molecular mechanisms are unknown. This study tried to investigate the influence of Sevo on hepatocellular carcinoma (HCC) cells and its possible mechanisms of action. The present study found that Sevo suppressed both the proliferative and invasive capabilities of both HCCLM3 and Huh7 cells in a dose-dependent manner. Moreover, 53 differentially expressed microRNAs (miRNAs/miRs) in HCC cells that resulted from Sevo were screened out using miRNA microarray assay. In particular, miR-25-3p displayed a significant decrease in response to Sevo treatment. Further studies showed that Sevo's inhibitory actions on HCC cells were attenuated by overexpression of miR-25-3p but enhanced by its inhibitor. Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN (PTEN), a tumor suppressor gene, was directly targeted by miR-25-3p and its expression was upregulated by Sevo. In addition, Sevo suppressed the expression of phosphorylated-protein kinase B (p-Akt) (S473), glycogen synthase kinase (GSK) 3β (p-GSK3β) (S9), β-catenin, c-Myc and matrix metalloproteinase 9; whereas these inhibitory effects were reversed by miR-25-3p overexpression. More importantly, Sevo's tumor-suppressive effects were enhanced by LY294002 (a PI3-kinase inhibitor) but weakened by insulin growth factor-1 (an agonist of the Akt signaling pathway). These data suggest that Sevo's antitumor effects on HCC could be explained, in part, by Sevo inhibiting the miR-25-3p/PTEN/Akt/GSK-3β/β-catenin signaling pathway.

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miR-25 promotes glioma cell proliferation by targeting CDKN1C

Cited by 39 publications

References 38 publications

Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation

Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation

Upregulation of microRNA-25-3p inhibits proliferation, migration and invasion of osteosarcoma cells in vitro by directly targeting SOX4

Sevoflurane inhibits the proliferation and invasion of hepatocellular carcinoma cells through regulating the PTEN/Akt/GSK‑3β/β‑catenin signaling pathway by downregulating miR‑25‑3p

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