lncRNA MAGI2-AS3 Research Articles

Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis.

BackgroundLung squamous cell carcinoma (LUSC) accounts for approximately 30% of all lung cancers that possesses the highest occurrence and mortality in all cancer types. Long noncoding RNAs have been reported to modulate tumor development for several decades.Aim of the StudyThis research aims to investigate the role of MAGI2-AS3 in LUSC.MethodsRT-qPCR tested genes (including MAGI2-AS3, miR-374a/b-5p and CADM2) expression. Cell proliferation was detected by colony formation and EdU assays. Cell migration and invasion were evaluated by transwell assay. Flow cytometry analysis of apoptotic cells and Western blot analysis on apoptosis-related genes were applied to measure cell apoptosis. Nuclear-cytoplasmic fractionation and FISH assay positioned MAGI2-AS3. The combination between miR-374a/b-5p and MAGI2-AS3 (or CADM2) was determined by luciferase reporter assay and RIP assay.ResultsMAGI2-AS3 inhibited the proliferative, migratory and invasive capability of LUSC cells with upregulated expression. Additionally, MAGI2-AS3 overexpression promoted cell apoptosis. We discovered that MAGI2-AS3 was located in the cytoplasm. Hereafter, we found out that MAGI2-AS3 targeted miR-374a/b-5p. CADM2 was targeted by miR-374a/b-5p. Finally, rescue assays indicated that the promoting effects of miR-374a/b-5p amplification on biological activities were restored by CADM2 addition.ConclusionIn conclusion, lncRNA MAGI2-AS3 suppressed LUSC by regulating miR-374a/b-5p/CADM2 axis, which might potentially serve as a therapeutic marker for LUSC patients.

Overexpression of lncRNA MAGI2-AS3 Retards Tumor Progression and Angiogenesis by Regulating ACY1 via Interacting with Transcription Factor HEY1

Overexpression of lncRNA MAGI2-AS3 Retards Tumor Progression and Angiogenesis by Regulating ACY1 via Interacting with Transcription Factor HEY1

LncRNA MAGI2-AS3 is involved in cervical squamous cell carcinoma development through CDK6 up-regulation

BackgroundIt has been reported that lncRNA MAGI2-AS3 can promote many types of cancer, such as breast cancer and bladder cancer, by regulating cell behaviors, such a proliferation, invasion, and migration. However, its role in cervical squamous cell carcinoma (CSCC) is unclear. This study aims to investigate the role of MAGI2-AS3 in CSCC.MethodsSixty-four CSCC patients (36 to 68 years, 46.3 ± 5.1 years) out of 136 CSCC patients admitted by Shengjing hospital affiliated to China Medical University from June 2010 to October 2013 were included in the present study. Among the 64 enrolled patients, 20 were HPV-16 positive cases, 24 were HPV-18 positive cases and 20 were HPV negative. CSCC and non-tumor biopsies from CSCC patients as well as C-33A cell lines were used. Cells were transfected with MAGI2-AS3 and CDK6 expression vectors as well as with MAGI2-AS3 siRNA to analyze gene interactions. Cell cycle analysis was performed to analyze the effects of transfections on cell cycle progression. qPCR and western blot were applied to analyze gene expression. Paired t-test and ANOVA (one-way) combined with Tukey test were used for data comparisons. Survival analysis was performed by plotting and comparing survival curves.ResultsqRT-PCR results showed that CDK6 and MAGI2-AS3 were both up-regulated in CSCC and positively correlated with each other. MAGI2-AS3 and CDK6 expression was not significantly affected by HPV infections. High levels of MAGI2-AS3 were associated with the poor survival of CSCC patients. In CSCC cells, MAGI2-AS3 over-expression up-regulated CDK6, while MAGI2-AS3 siRNA down-regulated CDK6. In CCK-8 assay, MAGI2-AS3 and CDK6 over-expression led to increased proliferation rate of CSCC cells by reducing CDK6 levels, while MAGI2-AS3 siRNA didn’t. In addition, CDK6 over-expression attenuated the effect of MAGI2-AS3 siRNA silencing.ConclusionsIn conclusion, MAGI2-AS3 promoted CSCC cell proliferation by up-regulating CDK6.

LncRNA MAGI2-AS3 Is Regulated by BRD4 and Promotes Gastric Cancer Progression via Maintaining ZEB1 Overexpression by Sponging miR-141/200a

Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and tumor progression. However, the biological function of most lncRNAs remains unknown in human gastric cancer. This study here aims to explore the unknown function of lncRNA MAGI2-AS3 in gastric cancer. First, bioinformatics analysis showed that lncRNA MAGI2-AS3 was overexpressed in gastric cancer tissues, and the overexpression of MAGI2-AS3 has been shown to be associated with poor prognosis in all three independent gastric cancer cohorts (The Cancer Genome Atlas stomach cancer [TCGA_STAD], GEO: GSE62254 and GSE15459). The multivariate analysis indicated that lncRNA MAGI2-AS3 was an independent prognostic factor for both overall survival and disease-free survival of gastric cancer patients. Moreover, MAGI2-AS3 was identified to be an epithelial-mesenchymal transition (EMT)-related lncRNA and was highly co-expressed with ZEB1/2 in both gastric cancer tissues and normal stomach tissues. Loss-of-function and gain-of-function studies showed that lncRNA MAGI2-AS3 could positively regulate ZEB1 expression and the process of cell migration and invasion in gastric cancer. Subcellular location assay showed that lncRNA MAGI2-AS3 was mainly located in the cytoplasm of gastric cancer cells. Bioinformatics analysis and functional experiments revealed that lncRNA MAGI2-AS3 was negatively correlated with miR-141/200a expression and negatively regulated miR-141/200a-3p expression in gastric cancer. Therefore, we speculate that lncRNA MAGI2-AS3 promotes tumor progression through sponging miR-141/200a and maintaining overexpression of ZEB1 in gastric cancer. Nevertheless, we identified that BRD4 is a transcriptional regulator of lncRNA MAGI2-AS3 in gastric cancer. Additionally, our findings highlight that lncRNA MAGI2-AS3 is an ideal biomarker and could be a potential therapeutic target for gastric cancer.

Hypomethylation of the lncRNA SOX21-AS1 has clinical prognostic value in cervical cancer

AimsCervical cancer seriously affects women's health. The function of methylated alterations in the long non-coding RNAs (lncRNAs) promote the progression and metastasis of cancer. Our study aims to identify the functional effects of lncRNA methylation in cervical carcinogenesis. Main methodsGenome-wide DNA methylation of 6 samples was assessed using the Illumina Infinium MethylationEPIC BeadChip. RNA sequencing (RNA-seq) data and survival follow-up time of 307 samples from The Cancer Genome Atlas (TCGA) dataset were enrolled in this study. The statistical analysis and graphical work were mainly realized by R language. Key findingsMethylation map identified 3962 hypermethylated CpG sites and 4484 hypomethylated CpG sites in cervical cancer (|Δβ| ≥ 0.20). Bioinformatic analysis of the lncRNA expression identified 363 upregulated and 664 downregulated lncRNAs with log2 (fold change) ≥ 1.00 in squamous cervical carcinoma (SCC) samples. Weighted gene co-expression network analysis (WGCNA) and Venn diagram revealed that lncRNA MAGI2 antisense RNA 3 (lncRNA MAGI2-AS3), lncRNA WT1 antisense RNA (lncRNA WT1-AS) and lncRNA SOX21 antisense divergent transcript 1 (lncRNA SOX21-AS1) were important methylation changed lncRNAs. Kaplan-Meier survival curves showed only lncRNA SOX21-AS1 had clinical prognostic value in cervical cancer. Gene set enrichment analysis (GSEA) suggest that lncRNA SOX21-AS1 involve in the multiple cellular processes and might significantly suppress cervical tumorigenesis. SignificanceThese insights into the functional role of lncRNA SOX21-AS1 DNA methylome alterations in cervical cancer might promote clinically new applicable in diagnosis and prognosis.

Long non-coding RNA MAGI2-AS3 inhibits breast cancer cell migration and invasion via sponging microRNA-374a.

Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts that play important roles in tumorigenesis and tumor progression. Our study aimed to explore the role of lncRNA MAGI2-AS3 in breast cancer metastatic progression. In the present study, our results showed that MAGI2-AS3 can inhibit the migration and invasion of breast cancer cells. In addition, an increase in MAGI2-AS3 can inhibit microRNA-374a (miR-374a) expression in breast cancer cells. Bioinformatic analysis predicted the correlation between MAGI2-AS3 and miR-374a. Phosphatase and tensin homolog (PTEN) was found to be an novel mRNA target of miR-374a. MAGI2-AS3 upregulation inhibited breast cancer metastatic progression by decreasing miR-374a and enhancing PTEN expression. Together, our data revealed that lncRNA MAGI2-AS3 is involved in breast cancer cell progression by regulating the miR-374a-PTEN axis. These findings offer new insight into treatment strategies for breast cancer.

LncRNA MAGI2-AS3 inhibits hepatocellular carcinoma cell proliferation and migration by targeting the miR-374b-5p/SMG1 signaling pathway.

Long noncoding RNAs (lncRNAs) have been proven to play critical roles in cancer progression. Recently, lncRNA MAGI2-AS3 has been revealed to be a tumor suppressor and inhibit cell growth by targeting the Fas/FasL signalling pathway in breast cancer. However, the role and underlying mechanism of MAGI2-AS3 in hepatocellular carcinoma (HCC) remain largely unknown. In the current study, we found that MAGI2-AS3 expression is downregulated in HCC tissues and closely associated with some clinical characteristics (tumor size, lymph node metastasis, and TNM stage) and poor overall survival. Overexpression of MAGI2-AS3 inhibits HCC cell proliferation and migration in vitro, while impedes tumor growth in vivo accordantly. In addition, our data suggest that MAGI2-AS3 could function as an endogenous sponge of miR-374b-5p by directly binding to it and suppressing its expression. Furthermore, miR-374b-5p upregulation could restore the inhibitory effect of MAGI2-AS3 on HCC cells processes. Moreover, suppressor with morphogenetic effect on genitalia family member 1 (SMG1) is positively regulated by MAGI2-AS3 via absorbing miR-374b-5p in HCC cells. More important, SMG1 knockdown reverses the suppressive function of MAGI2-AS3 in HCC cell processes. Taken together, we reveal a functional MAGI2-AS3/miR-374b-5p/SMG1 axis that suppresses HCC progression, potently suggesting a new road for HCC treatment.

Long noncoding RNA MAGI2-AS3 regulates CCDC19 expression by sponging miR-15b-5p and suppresses bladder cancer progression

Bladder cancer (BCa) belongs to a popular urological malignancy and leads to large numbers of deaths worldwide. Recently, emerging evidences indicate that long noncoding RNAs (lncRNAs) are closely related with BC occurrence and progression. However, the function of lncRNA MAGI2-AS3 remains poorly understood in BC. In this present study, we screened out a novel lncRNA MAGI2-AS3 whose expression was downregulated in BCa tissues. We showed that MAGI2-AS3 downregulation in BCa patients indicated a poor prognosis. Functionally, we showed that MAGI2-AS3 overexpression inhibits proliferation, migration and invasion of BCa cells. Moreover, ectopic expression of MAGI2-AS3 suppresses BCa growth in vivo. Bioinformatics analysis revealed that MAGI2-AS3 could serve as a competing endogenous RNA (ceRNA) for miR-15b-5p. In the meantime, miR-15b-5p directly targeted CCDC19, a tumor suppressor in BCa. Rescue assays demonstrated that knockdown of CCDC19 restored the proliferation, migration and invasion of BCa cells suppressed by MAGI2-AS3 overexpression. In conclusion, this study identified a novel mechanism that MAGI2-AS3/miR-15b-5p/CCDC19 signaling pathway regulates BCa progression.

Long non-coding RNA (lncRNA) MAGI2-AS3 inhibits breast cancer cell growth by targeting the Fas/FasL signalling pathway.

Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts shown to play important roles in tumourigenesis and tumour progression. Our study aimed to examine expression of the lncRNA MAGI2-AS3 in breast cancer and to explore its function in cancer cell growth. First, MAGI2-AS3 expression levels in clinical samples and cell lines were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The functional significance of MAGI2-AS3 in cancer cell proliferation and apoptosis was then examined in vitro. Our results showed MAGI2-AS3 to be down-regulated in breast cancer tissues compared to normal adjacent tissues. Moreover, MAGI2-AS3 markedly inhibited breast cancer cell growth and increased expression of Fas and Fas ligand (FasL). In conclusion, our data suggest that MAGI2-AS3 expression is decreased in breast cancer and that MAGI2-AS3 plays an important role as a tumour suppressor by targeting Fas and FasL signalling. These results provide new insight into novel clinical treatments for breast cancer.