EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma

Lian, Rong; Ma, Huimin; Wu, Zhiyan; Zhang, Guozheng; Jiao, Lei; Miao, Wenjie; Jin, Qianqian; Li, Ruixue; Chen, Ping; Shi, Haixu; Yu, Wenfa

doi:10.1007/s11010-017-3133-7

Cited by 17 publications

(18 citation statements)

References 39 publications

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“…The pro-proliferative role of EZH2 in cancer cells is also well established. Lian et al (35) demonstrated that EZH2 promotes laryngeal cancer cell proliferation by regulating Runt-related transcription factor 3 expression. Additionally, the inhibition of EZH2 by a small-molecule inhibitor suppresses tumor cell growth via induction of the tumor-suppressor protein p16 INK4A (36).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑101‑3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9

Chen

et al. 2018

Exp Ther Med

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Retinoblastoma is the most frequent intraocular malignant tumor type to occur in childhood. MicroRNA (miR)-101-3p has been reported to function as a tumor suppressor in various types of cancer. However, the biological function and underlying mechanisms of miR-101-3p in retinoblastoma are largely unknown. In the present study, it was identified that miR-101-3p was downregulated in retinoblastoma. MTT and flow cytometry assays demonstrated that ectopic overexpression of miR-101-3p significantly inhibited cell viability and cell cycle progression in WERI-Rb-1 and Y79 cells. In vivo mouse experiments further confirmed the anti-proliferative role of miR-101-3p in retinoblastoma. Additionally, predictions with TargetScan software indicated that the 3′-untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. Accordingly, a dual luciferase reporter gene assay demonstrated that miR-101-3p directly targeted EZH2 and HDAC9 to suppress the proliferation of retinoblastoma cells. Meanwhile, the restoration of EZH2 or HDAC9 expression countered the anti-proliferative effect of miR-101-3p on WERI-Rb-1 and Y79 cells. Collectively, these data highlight the role of miR-101-3p in the tumorigenesis of retinoblastoma, and indicate its suitability as a novel therapeutic target.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑101‑3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9

Chen

et al. 2018

Exp Ther Med

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“…EZH2 was verified to contribute to the aggressiveness of various human cancers [ 15 ]. For example, EZH2 promotes cell proliferation in laryngeal carcinoma [ 16 ], inducing cell metastasis in oral cancer [ 17 ], increasing cell invasion in endometrial cancer [ 18 ] Dysregulation of EZH2 in HCC has been found in some studies. For instance, up-regulated EZH2 was measured in HCC tissues, which was positively correlated with tumor grade and clinical stage [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PVT1 modulates hepatocellular carcinoma cell proliferation and apoptosis by recruiting EZH2

Jian-ping¹,

Hao

Wang

et al. 2018

Cancer Cell Int

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BackgroundWe aimed to figure out the molecular network of PVT1 and EZH2 on hepatocellular carcinoma (HCC) cells growth. We also explored the interaction between PVT1, EZH2, MDM2 and P53.MethodsMicroarray analysis was performed to screen for abnormally expressed genes in HCC tissues and PVT1 was identified as one gene significantly upregulated in HCC. CCK-8 assay, colony formation assay, and flow cytometry detected cell vitality, proliferation and apoptosis, respectively. RIP and RNA pull-down assays were employed to examine the connection between PVT1 and EZH2. The effect of PVT1 on the stability of EZH2 protein and the impact of EZH2 on MDM2 were detected by ELISA. Co-immunoprecipitation assay was used to evaluate the relationship between MDM2 and EZH2. Western blot detected the expression of EZH2, MDM2 and P53.ResultsUp-regulated PVT1 was detected in HCC. Knockdown of PVT1 inhibited HCC cell propagation and promoted apoptotic cells. PVT1 could improve EZH2 protein stability by binding to EZH2 protein but have no significant impact on EZH2 mRNA expression. EZH2 protein stabilized MDM2 protein expression by binding to MDM2 protein. PVT1 enhanced the protein expression of EZH2 and MDM2 as well as inhibited P53 protein expression.ConclusionsPVT1 promoted HCC cell propagation and inhibited apoptotic cells by recruiting EZH2, stabilizing MDM2 protein expression and restraining P53 expression.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0582-3) contains supplementary material, which is available to authorized users.

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“…Moreover, our study revealed that EZH2 expression was remarkably upregulated and EZH2 up-regulation abrogated miR-101-mediated anti-autophagy, anti-proliferation and pro-apoptosis effect in LSCC cells. Consistently, EZH2 has been reported to be highly expressed in LSCC tissues and EZH2 overexpression facilitated the tumorigenesis of LSCC [19][20][21].…”

Section: Discussionmentioning

confidence: 58%

“…Next, TargetScan online website was used to predict possible targets of miR-101. Among candidate targets of miR-101, EZH2 was chosen because of its potential oncogenic roles in LSCC [19][20][21] (Figure 3A). To further confirm this predic-…”

Section: Mirmentioning

confidence: 99%

MicroRNA-101 regulates autophagy, proliferation and apoptosis via targeting EZH2 in laryngeal squamous cell carcinoma

Chen

Jia

Zang

et al. 2019

neo

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Laryngeal carcinoma is the second commonest head and neck carcinoma globally. MicroRNA-101 (miR-101) has been reported as a tumor suppressor in multiple malignancies including laryngeal squamous cell carcinoma (LSCC). However, the roles and molecular mechanisms of miR-101 in the development of LSCC have not been fully elucidated. In the present study, RT-qPCR assay was performed to detect the expression of miR-101 and enhancer of zeste homolog 2 (EZH2) mRNA. Western blot assay was conducted to determine protein expression of LC3-I, LC3-II, p62 and EZH2. Cell proliferative capacity was evaluated by MTS assay. The effect of miR-101 alone or along with EZH2 on cell apoptosis was assessed by apoptotic index and caspase-3 activity. Bioinformatic analysis, luciferase assay and RNA immunoprecipitation (RIP) assay were carried out to investigate the interaction between miR-101 and EZH2. Results revealed that miR-101 expression was strikingly down-regulated in LSCC cell lines. Functional analyses showed that ectopic expression of miR-101 suppressed cell autophagy and proliferation and facilitated cell apoptosis in LSCC. Further investigations revealed that miR-101 inhibited EZH2 expression by direct interaction and EZH2 was highly expressed in LSCC cells. Also, EZH2 knockdown reduced the autophagic activity of LSCC cells. Moreover, restoration experiments showed that EZH2 up-regulation weakened miR-101mediated anti-autophagy, anti-proliferation and pro-apoptosis effects in LSCC cells. In conclusion, our findings suggested that miR-101 inhibited autophagy and proliferation and promoted apoptosis via targeting EZH2 in LSCC, providing a deep insight into the pathogenesis of LSCC and hinting the pivotal roles of epigenetic modifications especially histone methylation in the development of LSCC.

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EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma

Cited by 17 publications

References 39 publications

MicroRNA‑101‑3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9

MicroRNA‑101‑3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9

Long noncoding RNA PVT1 modulates hepatocellular carcinoma cell proliferation and apoptosis by recruiting EZH2

MicroRNA-101 regulates autophagy, proliferation and apoptosis via targeting EZH2 in laryngeal squamous cell carcinoma

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