miR-139 Functions as An Antioncomir to Repress Glioma Progression Through Targeting IGF-1 R, AMY-1, and PGC-1β

Wang, Hong; Yan, Xin; Ji, Lei; Ji, Xituan; Wang, Ping; Guo, Shiwen; Li, Sanzhong

doi:10.1177/1533034616630866

Cited by 26 publications

(29 citation statements)

References 43 publications

(50 reference statements)

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“…Jung and Kim (15) reported that the upregulation of MYCBP in colon carcinoma cells may have co-activating effects on MYC. Wang et al (20) reported that MYCBP regulated multiple biological processes within glioma cells, which is associated with malignant characteristics, including cancer cell proliferation, transformation and metastasis. Additionally, Furusawa et al (24) suggested that MYCBP is a trigger in the tumorigenesis of chronic myeloid leukemia.…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of MYC has been suggested to serve key roles in cell migration and invasion by promoting the expression of target genes (26). Previous studies have been performed to inhibit the expression of MYCBP, and thus the MYC pathway, and observe the resultant inhibition of cancer cell migration and invasion (20,27). Furthermore, the overexpression of MYCBP facilitated Hedgehog signaling responses, whereas the knockdown of MYCBP compromised Hedgehog signaling responses (28).…”

Section: Discussionmentioning

confidence: 99%

“…A previous study observed that the transcription of a series of target genes within the Wnt/β-catenin signaling pathway was activated following the formation of a TCF/LEF/β-catenin complex in the nucleus, which regulated cellular biological activities and promoted the migratory and invasive abilities of tumor cells (19). Recent studies have also indicated that MYCBP is associated with tumorigenesis in a variety of tumor types, including colon cancer and glioma (20,21). However, the potential role of MYCBP in promoting the growth of GC has, to the best of our knowledge, not been reported.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of MYC binding protein promotes invasion and migration in gastric cancer

et al. 2018

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Abstract. Gastric cancer (GC) is the second leading cause of cancer-associated mortality worldwide. Although the mortality rate of patients with GC has improved, it remains a significant health issue. The MYC proto-oncogene protein serves key roles in cellular proliferation, differentiation, transformation and apoptosis. Previous studies have identified the abnormal expression of MYC-binding protein (MYCBP) during tumorigenesis in multiple types of cancer. Furthermore, evidence demonstrates that the abnormal expression of MYCBP contributes to the invasion and migration of human cancer types, including colon cancer and glioma; however, its influence on GC remains unclear. In the present study, the expression of MYCBP in GC cells and tissues was analyzed by reverse transcription-quantitative polymerase chain reaction. Additionally, GC cell lines were transfected with small interfering RNAs against MYCBP or lymphoid enhancer-binding factor 1 (LEF-1) and assessed by in vitro transwell migration and invasion assays. The results indicated that the expression of MYCBP in GC cells and tissues was markedly increased compared with a normal gastric epithelial cell line and adjacent normal gastric mucosal tissues, respectively. Furthermore, MYCBP downregulation notably inhibited the metastatic capacity of GC cells, and LEF-1 knockdown was found to downregulate the expression of MYCBP. On the basis of the findings of the present study, MYCBP may be a direct target of the β-catenin/LEF-1 pathway via binding LEF-1, and could potentially be used as a biomarker for the diagnosis and prognosis of GC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Overexpression of MYC binding protein promotes invasion and migration in gastric cancer

et al. 2018

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“…miR-378-and miR-378*-deficient mice are resistant to HFD-induced obesity and exhibit increased mitochondrial fatty acid metabolism (54). Second, PGC-1b is a direct target of miR-139 and may be involved in the development and progression of glioma cells (55). We also found that in response to OA treatment, miR-98-5p inhibited PGC-1b mRNA expression in the liver.…”

Section: Discussionmentioning

confidence: 64%

Hypolipidemic effect of oleanolic acid is mediated by the miR‐98‐5p/PGC‐1β axis in high‐fat diet‐induced hyperlipidemic mice

et al. 2016

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Oleanolic acid (OA) is an active component of the traditional Chinese herb and has been found to exhibit a significant lipid-lowering effect; however, its direct molecular target is still unknown, which limits its clinical application and the possible structure modification to improve its beneficial functions. In this regard, we carried out the present study to identify potential hepatic targets of OA to mediate its lipid-lowering effect. We found that both acute and chronic OA treatments reduced serum levels of triglycerides, total cholesterol, and LDL cholesterol, and decreased hepatic expression levels of peroxisome proliferator-activated receptor-γ coactivator-1β (PGC-1β), which is an important regulator in maintaining hepatic lipid homeostasis, and its downstream target genes. Of note, liver-specific knockdown of PGC-1β recapitulated the hypolipidemic effects of OA. At the molecular level, OA accelerated mRNA degradation of PGC-1β. Microarray analysis revealed a host of microRNAs that potentially mediate OA-induced PGC-1β mRNA degradation, among which, miR-98-5p significantly inhibited activity of 3' UTR as well as PGC-1β expression and promoted its mRNA degradation. Conversely, miR-98-5p inhibitors blunted the inhibitory effects of OA on PGC-1β expression. Collectively, our data demonstrated that OA ameliorated hyperlipidemia, likely regulation of the miR-98-5p/PGC-1β axis.-Chen, S., Wen, X., Zhang, W., Wang, C., Liu, J., Liu, C. Hypolipidemic effect of oleanolic acid is mediated by the miR-98-5p/PGC-1β axis in high-fat diet-induced hyperlipidemic mice.

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“…Some miRNAs promoted gliomas development, which were considered as biomarkers for earlier diagnosis 16 . While another group of miRNAs functioned as anti-tumor genes and predicted better prognosis, such as miR-139, miR-124 and miR-34 [17][18][19] . Therefore identification glioma-related miRNAs and elucidation their effects and regulatory mechanisms have important roles in gliomas therapy.…”

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confidence: 99%

MicroRNA-144 represses gliomas progression and elevates susceptibility to Temozolomide by targeting CAV2 and FGF7

Liu

Ren

Zhao

et al. 2020

Sci Rep

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Malignant gliomas are the most common tumor in central nervous system with poor prognosis. Due to the limitation of histological classification in earlier diagnosis and individualized medicine, it is necessary to combine the molecular signatures and the pathological characteristics of gliomas. Lots of microRNAs presented abnormal expression in gliomas and modulated gliomas development.Exploration the miRNAs profile is helpful for the diagnosis, therapy and prognosis of gliomas. It has been demonstrated that miR-144 plays important roles in solid tumors. However, the detail mechanisms remained unrevealed. In this study, we have demonstrated the level of miR-144 decreased in glioma tissues from patients, especially in gliomas with higher grades. MiR-144 was also validated have lower expression in glioma cell lines compared with cortical neuron cell by using qRT-PCR. The in vitro functional experiment indicated miR-144 improved gliomas progression through repressing proliferation, sensitizing to chemotherapeutics and inhibiting metastasis. We further identified fibroblast growth factor 7 (FGF7) and Caveolin 2 (CAV2) were target genes of miR-144 by luciferase reporter assay and western blotting. The mechanisms study suggested forced FGF7 expression elevated Akt activation and decreased reactive oxygen species (ROS) generation. The MTT and cell cycle assay indicated miR-144 suppressed glioma cells proliferation through modulating FGF mediated Akt signaling pathway. Meanwhile, miR-144 promoted Temozolomide (TMZ) induced apoptosis in glioma cells via increasing ROS production by using FACS. On the other hand, CAV2, as another target of miR-144, accelerated glioma cells migration and invasion via promoting glioma cells EMT progress. Retrieved expression of FGF7 or CAV2 rescued the proliferation and migration function mediated by miR-144. Furthermore, the in vivo experiments in PDX models displayed the anti-tumor function of miR-144, which could be retrieved by overexpression of FGF7 and CAV2. Taken together, these findings indicated miR-144 acted as a potential target against gliomas progression and uncovered a novel regulatory mechanism, which may provide a new therapeutic strategy and prognostic indicator for gliomas.

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miR-139 Functions as An Antioncomir to Repress Glioma Progression Through Targeting IGF-1 R, AMY-1, and PGC-1β

Cited by 26 publications

References 43 publications

Overexpression of MYC binding protein promotes invasion and migration in gastric cancer

Overexpression of MYC binding protein promotes invasion and migration in gastric cancer

Hypolipidemic effect of oleanolic acid is mediated by the miR‐98‐5p/PGC‐1β axis in high‐fat diet‐induced hyperlipidemic mice

MicroRNA-144 represses gliomas progression and elevates susceptibility to Temozolomide by targeting CAV2 and FGF7

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