LncRNA MAFG-AS1 Promotes Lung Adenocarcinoma Cell Migration and Invasion by Targeting miR-3196 and Regulating SOX12 Expression.

Lung adenocarcinoma (LUAD) patients exhibit poor prognosis, primarily due to metastasis. Emerging studies have demonstrated that long noncoding RNAs (lncRNAs) play critical roles in cancer progression and metastasis besides their physiological function. Here, we investigated the potential role of lncRNA MAF BZIP Transcription Factor G Antisense RNA 1 (MAFG-AS1) in LUAD metastasis by analyzing its expression in The Cancer Genome Atlas (TCGA) LUAD database, and its function in LUAD using in vitro and in vivo experiments. We performed bioinformatics analysis, western blotting, dual-luciferase reporter gene assay, RNA immunoprecipitation (RIP), and rescue assays to reveal the molecular mechanisms underlying MAFG-AS1 function. We observed augmented expression of MAFG-AS1 in LUAD tissues compared with normal adjacent tissues, and its association with poor prognosis. Furthermore, MAFG-AS1 overexpression promoted LUAD cell migration, proliferation, invasion, and epithelial mesenchymal transition (EMT). Besides, MAFG-AS1 also targeted miR-3196 directly by acting as an endogenous sponge, thereby rescuing the inhibition of SOX12, a target of miR-3196. Thus, the rescue assays demonstrated that MAFG-AS1 promotes cell migration, invasion, and EMT by modulating the miR-3196/SOX12 pathway. In conclusion, our findings suggest that MAFG-AS1/miR-3196/SOX12 axis regulates LUAD progression and is a potential therapeutic target for LUAD.

Wu Q ，Jiang J 《-》

LncRNA MAFG-AS1 boosts the proliferation of lung adenocarcinoma cells via regulating miR-744-5p/MAFG axis.

Lung adenocarcinoma (LUAD) is typically featured by a low 5-year survival rate, hence there is a necessary to investigate new biomarkers in LUAD progression. Competing endogenous RNA (ceRNA) network has been widely reported in the regulation of tumor processes, which is also the main direction of this paper. Based on the data of GEPIA database, lncRNA MAFG-AS1 was upregulated in LUAD tissues, which was associated with poor prognosis of patients. Proliferation or apoptosis of LUAD cells were measured by CCK-8, EdU and caspase-3 activity assays followed by Western blot. The results indicated that silencing of MAFG-AS1 suppressed cell proliferation but induced cell apoptosis. RNA FISH staining showing the cytoplasmic localization of MAFG-AS1 in LUAD cells. Mechanism detection revealed that MAFG-AS1 served as a molecular sponge of miR-744-5p to upregulate its nearby gene MAF bZIP transcription factor G (MAFG) in LUAD cells. Functionally, MAFG overexpression attenuated the cellular processes mediated by MAFG-AS1 knockdown. In summary, this study unveiled the MAFG-AS1/miR-744-5p/MAFG axis in LUAD, providing a potent and promising therapeutic target for LUAD patients.

Sui Y ，Lin G ，Zheng Y ，Huang W ... -  《-》

LncRNA MAFG-AS1 facilitates the migration and invasion of NSCLC cell via sponging miR-339-5p from MMP15.

Non-small-cell carcinoma (NSCLC) is the most common cancer along with high mortality rate worldwide. In the present study, our data showed that lncRNA MAF BZIP Transcription Factor G Antisense RNA 1 (MAFG-AS1) was over-expressed in NSCLC tissues and cell lines. Overexpression of MAFG-AS1 promoted the migration, invasion and enhanced epithelial-mesenchymal transition (EMT) of NSCLC cell. In addition, miR-339-5p was predicted to be a target of MAFG-AS1 and the level of miR-339-5p was down-regulated in NSCLC. Over-expression of MAFG-AS1 significantly decreased the level of miR-339-5p in NSCLC cell. Moreover, the matrix metalloproteinase 15 (MMP15) was identified to be a target of miR-339-5p. The level of MMP15 was negatively regulated by miR-339-5p whereas positively controlled by MAFG-AS1. In addition, up-regulation of miR-339-5p neutralized the promoting impact of MAFG-AS1 on the migration, invasion and EMT of NSCLC cell. Finally, the xenograft model suggested that MAFG-AS1 promoted the metastasis of NSCLC cell in vivo. Altogether, we proved that MAFG-AS1-miR-339-5p-MMP15 axis might be a promising therapeutic target for the treatment of patients with NSCLC.

Jia YC ，Wang JY ，Liu YY ，Li B ，Guo H ，Zang AM ... -  《-》

Long non-coding RNA FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) targets microRNA-141-3p to regulate lung adenocarcinoma cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression.

Huang H ，Yang C ，Zhang Q ，Zhuo T ，Li X ，Li N ，Zhu L ，Luo C ，Gan J ，Wu Y ... -  《-》

LncRNA MAFG-AS1 Promotes the Progression of Bladder Cancer by Targeting the miR-143-3p/COX-2 Axis.

Long noncoding RNAs (lncRNAs) are potential biomarkers that are very important for the development of cancer. Studies show that lncRNAs are significantly correlated with the carcinogenesis and progression of bladder cancer (BLCA). In this research, we aimed at probing into the role of lncRNA MAFG-AS1 in the tumorigenesis of BLCA. RT-qPCR was employed to detect MAFG-AS1 expression in BLCA tissues and cells. MAFG-AS1 siRNA and overexpression plasmid were transfected into 5637 and T24 BLCA cell lines to inhibit or upregulate MAFG-AS1 expression, respectively, and then the regulatory functions of MAFG-AS1 on BLCA cell proliferation, migration, and invasion were assessed using cell counting kit-8 (CCK-8) assay, EdU method, and Transwell experiments, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation were conducted to validate the targeting relationships between MAFG-AS1 and miR-143-3p, and miR-143-3p and COX-2. In addition, miR-143-3p was repressed in MAFG-AS1-silenced 5637 and T24 cell lines, and the function of MAFG-AS1/miR-143-3p axis in BLCA cells was further evaluated. The regulatory effects of MAFG-AS1 and miR-143-3p on the expression of COX-2 protein were detected by Western blot. MAFG-AS1 was remarkably upregulated in BLCA patient tissues and cell lines, and its high expression was closely related to histological grade, tumor size, and lymph node metastasis. Silencing of MAFG-AS1 inhibited BLCA cell proliferation, metastasis, and invasion, while overexpression of MAFG-AS1 in BLCA cells had opposite biological effects. MAFG-AS1 was proved to target miR-143-3p to repress its expression. Moreover, it was confirmed that MAFG-AS1 and miR-143-3p could modulate COX-2 expression. The MAFG-AS1/miR-143-3p/COX-2 axis contributes to BLCA progression.

Li D ，Zhong S ，Zhu Z ，Jiang X ，Zhang J ，Gu J ，Chen F ... -  《-》