miR-483 is down-regulated in gastric cancer and suppresses cell proliferation, invasion and protein O-GlcNAcylation by targeting OGT

Yu, Fei; Zhou, Cuncai; Liu, Y B; Wang, B; Mao, Lei; Li, Y

doi:10.4149/neo_2018_170608n411

Cited by 20 publications

(15 citation statements)

References 33 publications

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“…miRNAs, including miR-7, miR-302c, miR-483, miR-371a-3p and miR-218, have been indicated to be involved in the GC progression. 19,26,[28][29][30] Our previous study demonstrated that miR-146a/b could markedly inhibit invasion and metastasis of GC cells. 15 MiR-146a/b down-regulating UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) resulted in the activation of several tumor suppressor genes.…”

Section: Discussionmentioning

confidence: 98%

“…4 E2F3 is frequently overexpressed in quite a few cancers and its decrease may block tumor progression. 7,26 E2F3 has been found to be implicated in thyroid cancer metastasis to lung and liver, but the specific mechanism remained undetermined. 8 The results from this study indicated that E2F3 was overexpressed in GC samples, and high level of E2F3 expression might tend to poor prognosis in GC folks.…”

Section: Discussionmentioning

confidence: 99%

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Regulation of E2F Transcription Factor 3 by microRNA-152 Modulates Gastric Cancer Invasion and Metastasis

Shi¹,

Zhu²,

Shen³

et al. 2020

CMAR

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Background: The transcription factor, E2F transcription factor 3 (E2F3), has been proved to modulate metastasis in multiple human cancers. The present study was aimed to expound the function and specific mechanism of E2F3 in gastric cancer (GC) progression. Materials and Methods: The expression of E2F3, microRNA-152 (miR-152) and PLK1 (polo-like kinase 1) in GC cell lines was detected by quantitative RT-PCR and Western blot. The roles of E2F3 and miR-152 in GC metastasis were classified using gain-of-function and loss-of-function assays. The miRNAs directly targeting E2F3 were identified by bioinformatics analysis and luciferase reporter experiment. Chromatin immunoprecipitation was carried out to reveal the correlation between E2F3 and PLK1. Results: E2F3 expression was frequently up-regulated in GC tissues, and its high expression might imply poor prognosis. Downregulation of E2F3 restrained GC migration and invasion in vitro and in vivo. Interestingly, we proved that miR-152 was an upstream regulator of E2F3. Moreover, miR-152 reduced E2F3 expression by directly targeting its 3ʹ-UTR, and then modulated GC metastasis via polo-like kinase 1 (PLK1) mediated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) signals. Conclusion: E2F3 plays a crucial role in GC progression and the newly discovered miR-152/E2F3/PLK1 axis provides a new underlying target for therapy of metastasis in GC patients.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Regulation of E2F Transcription Factor 3 by microRNA-152 Modulates Gastric Cancer Invasion and Metastasis

Shi¹,

Zhu²,

Shen³

et al. 2020

CMAR

View full text Add to dashboard Cite

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“…19,20 In fact, it has been reported that a variety of miRNAs can function as biomarkers for the diagnosis and prognosis of human gliomas. 21 In recent years, miR-483 has been demonstrated to be downregulated in colon cancer, hepatocellular carcinoma and gastric cancer, 9,12,22 while it was upregulated in anaplastic thyroid cancer and Wilms' Tumor, 23,24 suggesting that the expression of miR-483 is distinct in different types of cancers. In this study, we found that miR-483 was low expressed in glioma tissues compared to the paracancerous normal tissues.…”

Section: Discussionmentioning

confidence: 99%

“…11 In addition, miR-483 inhibited cell proliferation, invasion in gastric cancer via OGT. 12 However, the roles of miR-483 in the recurrence and metastasis of glioma remain unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR-483 Targeted SOX3 to Suppress Glioma Cell Migration, Invasion and Promote Cell Apoptosis

Lu¹,

Yu²,

Zhang³

et al. 2020

OTT

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Objective: Glioma is the most common malignant brain tumor that has high aggressiveness. The aim of this study was to investigate the potential therapeutic targets for gliomas. Materials and Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to calculate the expression of miRNA and genes. The connection between the expression of miR-483 and patients' overall survival rate was evaluated using Kaplan-Meier analysis. In addition, the underlying mechanism was detected using luciferase assay. Results: The expression level of miR-483 was significantly decreased in glioma tissue samples and cell lines, compared to the adjacent tissues and normal cell lines. Downregulation of miR-483 or upregulation of SOX3 was associated with overall survival of glioma patients. Additionally, overexpression of miR-483 promotes cell invasion and migration and inhibits apoptosis. In addition, miR-483 directly targeted to SOX3, and the expression of miR-483 has a negative correlation with SOX3 in glioma tissues. SOX3 reversed partial functions of miR-483 on cell migration, invasion, and promoted cell apoptosis in glioma. Conclusion: MiR-483 inhibited glioma cell migration, invasion, and promoted glioma cell apoptosis by targeting SOX3. MiR-483 maybe acted as a potential target for the treatment of glioma.

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“…In ovarian cell lines expressing wildtype p53, the high level of OGT/O-GlcNAcylation can stabilize the tumor suppressor p53, and stabilized p53 further promotes the acquisition of new pro-oncogenic activities including cell proliferation and metabolic changes, whereas the stabilization of p53 was not detected in cell lines with mutated p53 (36,37), indicating a role of O-GlcNAcylation in regulating ovarian cancer proliferation and progression. Moreover, data of aberrant OGT level in various cancer tissues is also collected and analyzed by UALCAN based on TCGA datasets ( Figure 1) (38)(39)(40). Taken together, the changes in OGT/O-GlcNAcylation level directly affect tumor occurrence and progression.…”

Section: Imbalanced O-glcnacylation In Cancer Cellsmentioning

confidence: 99%

Functional Analysis of O-GlcNAcylation in Cancer Metastasis

Jin

Qiu

et al. 2020

Front. Oncol.

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One common and reversible type of post-translational modification (PTM) is the addition of O-linked b-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation), and its dynamic balance is controlled by O-GlcNAc transferase (OGT) and glycoside hydrolase O-GlcNAcase (OGA) through the addition or removal of O-GlcNAc groups. A large amount of research data confirms that proteins regulated by O-GlcNAcylation play a pivotal role in cells. In particularly, imbalanced levels of OGT and O-GlcNAcylation have been found in various types of cancers. Recently, increasing evidence shows that imbalanced O-GlcNAcylation directly or indirectly impacts the process of cancer metastasis. This review summarizes the current understanding of the influence of O-GlcNAc-proteins on the regulation of cancer metastasis. It will provide a theoretical basis to further elucidate of the molecular mechanisms underlying cancer emergence and progression.

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miR-483 is down-regulated in gastric cancer and suppresses cell proliferation, invasion and protein O-GlcNAcylation by targeting OGT

Cited by 20 publications

References 33 publications

<p>Regulation of E2F Transcription Factor 3 by microRNA-152 Modulates Gastric Cancer Invasion and Metastasis</p>

<p>Regulation of E2F Transcription Factor 3 by microRNA-152 Modulates Gastric Cancer Invasion and Metastasis</p>

<p>MiR-483 Targeted SOX3 to Suppress Glioma Cell Migration, Invasion and Promote Cell Apoptosis</p>

Functional Analysis of O-GlcNAcylation in Cancer Metastasis

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