MiR-1204 promotes ovarian squamous cell carcinoma growth by increasing glucose uptake

Xu, Jia; Gu, Xihui; Yang, Xuelin; Meng, Yuejin

doi:10.1080/09168451.2018.1527208

Cited by 16 publications

(14 citation statements)

References 18 publications

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“…MiR-137 suppresses CXCL12 expression, inhibiting glioblastoma progression [22]. Interestingly, miR-1204 have been manifested to drive the progression of breast cancer and ovarian squamous cell carcinoma via regulating cell growth and EMT [24,39]. Nevertheless, the role of miR-1204 in GBM was poorly comprehended.…”

Section: Discussionmentioning

confidence: 99%

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CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

Zhao¹,

Shen²,

Ma³

et al. 2020

Cancer Cell Int

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Background: Glioblastoma (GBM) is a subclass of brain malignancy with unsatisfactory prognosis. MicroRNAs (miR-NAs) are a group of non-coding RNAs (ncRNAs) that exert key function on tumorigenesis and tumor development. Purposes: The purpose of this work was to unravel the biological behavior and mechanism of miR-1204 in GBM. Methods: Expressions of miR-1204, NR3C2 and CREB1 were detected by RT-qPCR and western blot. Proliferation and apoptosis of GBM cells were detected by CCK-8, colony formation, caspase-3 activity and TUNEL assays. Molecular interplays were examined by ChIP, RIP, and luciferase reporter assays. Results: MiR-1204 level was elevated in GBM cell lines. Functionally, miR-1204 aggravated cell proliferation whereas suppressed cell apoptosis in GBM cells. Mechanistically, cAMP Responsive Element Binding Protein 1 (CREB1) bound to the promoter of miR-1204 and activated the transcription of miR-1204. Furthermore, miR-1204 targeted and inhibited Nuclear receptor subfamily 3 group C member 2 (NR3C2), a tumor suppressor gene in GBM cells. Rescue assays indicated that NR3C2 participated in the regulation of miR-1204 on the malignant phenotype of GBM cells. Conclusions: We observed for the first time that CREB1-induced miR-1204 promoted malignant phenotype of GBM through targeting NR3C2, indicating that miR-1204 acted as a novel oncogenic miRNA in GBM.

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Section: Discussionmentioning

confidence: 99%

“…Further, the oncogenic role of miR-1204 in some cancers has been validated. For instance, miR-1204 contributes to cell growth in ovarian squamous cell carcinoma via increasing glucose uptake [24]. MiR-1204 promotes epithelialmesenchymal transition (EMT) and metastasis in breast cancer by targeting VDR [25].…”

Section: Introductionmentioning

confidence: 99%

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

Zhao¹,

Shen²,

Ma³

et al. 2020

Cancer Cell Int

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“…At present, few studies have been conducted in the investigation of hsa-miR-934 . For hsa-miR-1204 , Xu et al (43) revealed that hsa-miR-1204 expression was significantly correlated with tumour size. The expression levels of hsa-miR-1204 and glucose transporter-1 (GLUT-1) were significantly high in ovarian cancer (OC) patients (43).…”

Section: Discussionmentioning

confidence: 99%

“…For hsa-miR-1204 , Xu et al (43) revealed that hsa-miR-1204 expression was significantly correlated with tumour size. The expression levels of hsa-miR-1204 and glucose transporter-1 (GLUT-1) were significantly high in ovarian cancer (OC) patients (43). The expression levels of hsa-miR-1204 were positively correlated with the expression levels of GLUT-1 in OC patients.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential core genes and miRNAs in testicular seminoma via bioinformatics analysis

et al. 2019

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Testicular seminoma is one of the most common tumours in the field of urology, and its aetiology is still unclear. The aim of the present study was to identify the factors responsible for the development of testicular cancer and to investigate whether mutations in these genes were primarily congenital or acquired. To identify the key genes and miRNAs linked to testicular seminoma, as well as their potential molecular mechanisms, the GSE15220, GSE1818 and GSE59520 microarray datasets were analysed. A total of 5,195 and 1,163 differentially expressed genes (DEGs) were identified after analysing the GSE15220 and GSE1818 datasets, respectively. Among them, 287 genes were common between the two datasets. Of these, 110 were upregulated and 177 were downregulated. Five differentially expressed microRNAs (miRs; DEMs) that were downregulated in seminoma were identified after analysing the GSE59520 dataset. Following protein-protein interaction network and Gene Ontology analysis, the five nodes with the highest degrees were screened as hub genes. Among them, the high expression of hub genes, such as protein tyrosine phosphatase receptor type C (PTPRC), was associated with worse overall survival. We also predicted the potential target genes of the DEMs. DNA topoisomerase II α (TOP2A), marker of proliferation Ki-67 (MKI67), PTPRC and ubiquitin conjugating enzyme E2 C were associated with the PI3K/AKT and Wnt/β-catenin signalling pathways. In addition, hsa-miR-650 and hsa-miR-665 were associated with the PI3K/AKT and Wnt/β-catenin signalling pathways. Additionally, TOP2A and MKI67 were strongly associated with the target genes hsa-miR-650 and hsa-miR-665, respectively. We proposed that the hub genes reported in the present study may have a certain impact on cellular proliferation and migration in testicular seminoma. The roles of these hub genes in seminoma may provide novel insight to improve the diagnosis and treatment of patients with seminoma.

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“…For example, overexpression of miR-1207-5p reduces the expression of signal transducers and activators of transcription (STAT6), thereby activates cyclin-dependent kinase inhibitor 1A (CDKN1A) and CDKN1B to regulate the cell cycle and promote tumor cell proliferation (49). In addition, the elevated expression of miR-1204 not only significantly increases glucose transporters 1 (GLUT-1) expression and glucose uptake but also suppresses the expression of pitx1 and Vitamin D (1,25- dihydroxy vitamin D3) receptor (VDR), which ultimately promotes cell proliferation, invasion, and metastasis (50, 51). In addition, miR-1205 downregulates the expression of the Egl-9 family hypoxia-inducible factor 3 (EGLN3) and promotes cell proliferation and cell cycle progression and inhibits hydrogen peroxide-induced apoptosis (52).…”

Section: Pvt1 Regulates Tumor Progression Through Encoding Mirnasmentioning

confidence: 99%

PVT1 Promotes Cancer Progression via MicroRNAs

Wang

Zhou

et al. 2019

Front. Oncol.

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Non-coding RNA (ncRNA) plays a regulatory role in a variety of cellular activities. And long non-coding RNA (lncRNA) is one of the important kinds of ncRNA. Previous studies have shown that various lncRNAs are involved in the progression of cancer. LncRNA plasmacytoma variant translocation 1 (PVT1) is a newly discovered oncogenic factor that has been confirmed to be overexpressed in many cancer cells. Moreover, the role of PVT1 in cancer development is closely linked to microRNAs (miRNAs). PVT1 can act as a “sponge” for miRNAs to inhibit their activities, thereby affecting proliferation, invasion, and angiogenesis of cancer. In addition, PVT1 itself can be spliced and processed into several miRNAs such as miR-1204 and miR-1207, which can also regulate the development of cancer. This review summarizes various pathways through which PVT1 regulates the progression of cancer via miRNAs. We also propose additional regulatory mechanisms of PVT1 and their potential clinical applications.

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MiR-1204 promotes ovarian squamous cell carcinoma growth by increasing glucose uptake

Cited by 16 publications

References 18 publications

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

Identification of potential core genes and miRNAs in testicular seminoma via bioinformatics analysis

PVT1 Promotes Cancer Progression via MicroRNAs

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