MicroRNA-362-3p Targets PAX3 to Inhibit the Development of Glioma through Mediating Wnt/β-Catenin Pathway

Xu, Ganqiong; Fang, Pingping; Chen, Kanmin; Xu, Qingmei; Song, Zhen; Ouyang, Zhu

doi:10.1159/000499766

Cited by 13 publications

(5 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-362-3p has been shown to be abnormally expressed in a variety of tumors [21, 22]. For instance, it was reported that miR-362-3p, as a tumor suppressor, inhibited the progression of Glioma by targeting PAX3 and LUAD tumorigenesis by decreasing the E2F1, respectively [23, 24]. RAB23 is an important member of RAS proto-oncogene family and is considered as an tumor promoter [25].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p

Zeng

et al. 2019

Cancer Cell Int

View full text Add to dashboard Cite

Background CircRNA myosin light chain kinase (circRNA MYLK) has been shown to promote the progression of various tumor diseases. The purpose of this study was to explore the potential molecular mechanism of circMYLK in hepatocellular carcinoma (HCC). Methods The quantitative Real-Time PCR (qRT-PCR) was used to measure the expressions of circMYLK, miR-362-3p and Rab23 in HCC tissues and cell lines. Huh7 and Hep3B cells were selected to explore the role of circMYLK in proliferation, invasion and migration of HCC cells in vitro. The interaction among circMYLK, miR-362-3p and Rab23 was investigated by biological information and dual luciferase gene reporter assay. The effect of circMYLK on HCC tumor growth in vivo was studied in a tumor xenograft model in mice. Results CircMYLK was highly expressed in HCC tissues and cell lines, which was associated with poor prognosis in HCC patients. In addition, knockdown of circMYLK remarkably inhibited the proliferation, invasion, and migration of Huh7 and Hep3B cells. MiR-362-3p was a direct target of circMYLK, and Rab23 was a direct target gene of miR-362-3p. Meanwhile, circMYLK was negatively correlated with the expression of miR-362-3p and positively correlated with Rab23 expression. Moreover, either overexpressed miR-362-3p or silencing Rab23 could observably suppress the enhanced proliferation, invasion, and migration induced by circMYLK in Huh7 and Hep3B cells. Finally, knockdown of circMYLK and overexpressed miR-362-3p could suppress the expression of Rab23, thus inhibiting the growth and proliferation of Hep3B cells in vivo. Conclusion circMYLK promotes the occurrence and development of HCC by regulating the miR-362-3p/Rab23 axis, which provides a novel direction and theoretical basis for the early diagnosis and treatment of HCC.

show abstract

Section: Introductionmentioning

confidence: 99%

Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p

Zeng

et al. 2019

Cancer Cell Int

View full text Add to dashboard Cite

show abstract

“…For example, Xu et al have reported that miR-362-3p expression is decreased in glioma tissues and cells and can suppress the development of glioma. 19 A study by Wang et al reveals the downregulated expression of miR-362-3p in cervical adenocarcinoma tissues and cell lines, and reveals its inhibitory role in cervical adenocarcinoma. 20 In epithelial ovarian cancer (EOC), miR-362-3p levels are low in EOC tissues and cells, and play an anti-proliferative role in EOC.…”

Section: Discussionmentioning

confidence: 99%

Aberrant miR-362-3p is Associated with EBV-Infection and Prognosis in Nasopharyngeal Carcinoma and Involved in Tumor Progression by Targeting JMJD2A

Wang

Chen

2022

OTT

View full text Add to dashboard Cite

Background Many microRNAs (miRNAs) are involved in the progression of nasopharyngeal carcinoma (NPC). This study aimed to examine the expression and clinical significance of microRNA (miR)-362-3p in NPC, especially in Epstein–Barr virus (EBV)-positive patients, and explore its potential mechanism in NPC progression. Methods miR-362-3p levels and Jumonji C domain 2A (JMJD2A) mRNA levels were detected by quantitative real-time PCR. The diagnostic value of miR-362-3p to distinguish NPC patients and EBV-positive cases was evaluated using receiver operating characteristic analysis. The association of miR-362-3p with NPC survival was assessed by Kaplan–Meier curves and Cox regression analysis. NPC cell proliferation, migration and invasion were determined using Cell Counting Kit-8 and Transwell assays, respectively. A luciferase reporter assay was used to confirm the interaction between miR-362-3p and JMJD2A. Results miR-362-3p expression was decreased in the serum and tissues of NPC patients and had diagnostic value for screening NPC. According to the survival follow-up, NPC survivors had significantly higher miR-362-3p, and miR-326-3p was demonstrated as an independent prognostic indicator of NPC. Interestingly, it is found that EBV-positive NPC patients and cells had significantly lower miR-362-3p compared with EBV-negative NPC patients and cells and had certain ability to distinguish EBV-positive patients. Moreover, miR-362-3p inhibited the proliferation, migration and invasion of both EBV-positive and -negative NPC cells, and these effects might be mediated by targeting JMJD2A. Conclusion Abnormal miR-362-3p expression is related to EBV-infection and prognosis in NPC patients and may be involved in NPC progression by targeting JMJD2A.

show abstract

“…EMX1 and WASF2 levels should be further explored as potential clinical metrics in SCG for patient stratification and disease prognostication. Considering that the other member of the EMX family of transcription factors, EMX2, has been proposed to as a potential suppressor of GBM cells (Falcone et al., 2016 ; Monnier et al., 2018 ), and the WNT/β‐catenin pathway has been report linking to the malignant phonotype of brain glioma (Fan et al., 2021 ; Xiang et al., 2022 ; Xu et al., 2019 ), the EMX1/WASF2/β‐catenin possibly also can be applied to gliomas occurring in other locations such as the brain. We would like to focus on this issue in the future researches.…”

Section: Discussionmentioning

confidence: 99%

EMX1 functions as a tumor inhibitor in spinal cord glioma through transcriptional suppression of WASF2 and inactivation of the Wnt/β‐catenin axis

et al. 2022

View full text Add to dashboard Cite

Background: Gliomas are the most frequent and aggressive cancers in the central nervous system, and spinal cord glioma (SCG) is a rare class of the gliomas. Empty spiracles homobox genes (EMXs) have shown potential tumor suppressing roles in glioma, but the biological function of EMX1 in SCG is unclear. Methods:The EMX1 expression in clinical tissues of patients with SCG was examined. SCG cells were extracted from the tissues, and altered expression of EMX1 was then introduced to examine the role of EMX1 in cell growth and invasiveness in vitro.Xenograft tumors were induced in nude mice for in vivo validation. The targets of EXM1 were predicted via bioinformatic analysis and validated by luciferase and ChIP-qPCR assays. Rescue experiments were conducted to validate the involvements of the downstream molecules.Results: EMX1 was poorly expressed in glioma, which was linked to decreased survival rate of patients according to the bioinformatics prediction. In clinical tissues, EMX1 was poorly expressed in SCG, especially in the high-grade tissues. EMX1 upregulation significantly suppressed growth and metastasis of SCG cells in vitro and in vivo.EMX1 bound to the promoter of WASP family member 2 (WASF2) to suppress its transcription. Restoration of WASF2 blocked the tumor-suppressing effect of EMX1.EMX1 suppressed Wnt/β-catenin signaling activity by inhibiting WASF2. Coronaridine, a Wnt/β-catenin-specific antagonist, blocked SCG cell growth and metastasis induced by WASF2. Conclusion:This study elucidates that EMX1 functions as a tumor inhibitor in SCG by suppressing WASF2-dependent activation of the Wnt/β-catenin axis.

show abstract

MicroRNA-362-3p Targets PAX3 to Inhibit the Development of Glioma through Mediating Wnt/β-Catenin Pathway

Cited by 13 publications

References 28 publications

Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p

Circular RNA MYLK promotes hepatocellular carcinoma progression by increasing Rab23 expression by sponging miR-362-3p

Aberrant miR-362-3p is Associated with EBV-Infection and Prognosis in Nasopharyngeal Carcinoma and Involved in Tumor Progression by Targeting JMJD2A

EMX1 functions as a tumor inhibitor in spinal cord glioma through transcriptional suppression of WASF2 and inactivation of the Wnt/β‐catenin axis

Contact Info

Product

Resources

About