Dataset Information

LncRNA GACAT1 induces tongue squamous cell carcinoma migration and proliferation via miR-149.

ABSTRACT: Recent studies have observed that lncRNAs (long non-coding RNAs) are involved in the progression of various tumours including tongue squamous cell carcinoma (TSCC). Recently, a new lnRNA, GACAT1, has been firstly identified in gastric cancer. However, its potential role in TSCC remains unknown. In this reference, we observed that GACAT1 was overexpressed in TSCC samples and cell lines. Of 25 TSCC specimens, GACAT1 expression was overexpressed in 18 patients (18/25, 72%) compared to non-tumour specimens. Ectopic expression of GACAT1 induced cell growth and migration and promoted epithelial to mesenchymal transition in TSCC. In addition, ectopic expression of GACAT1 decreased miR-149 expression in SCC1 cell. We observed that miR-149 expression was down-regulated in TSCC cell lines. Moreover, we observed that GACAT1 expression was negatively correlated with miR-149 expression. GACAT1 overexpression induced TSCC cell growth and migration via regulating miR-149 expression. These data provided that GACAT1 played an oncogenic role in the progression of TSCC partly through modulating miR-149 expression.

SUBMITTER: Wang X

PROVIDER: S-EPMC8419168 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

LncRNA GACAT1 induces tongue squamous cell carcinoma migration and proliferation via miR-149.

Wang Xueling X Gong Zuode Z Ma Long L Wang Qibao Q

Journal of cellular and molecular medicine 20210810 17

Recent studies have observed that lncRNAs (long non-coding RNAs) are involved in the progression of various tumours including tongue squamous cell carcinoma (TSCC). Recently, a new lnRNA, GACAT1, has been firstly identified in gastric cancer. However, its potential role in TSCC remains unknown. In this reference, we observed that GACAT1 was overexpressed in TSCC samples and cell lines. Of 25 TSCC specimens, GACAT1 expression was overexpressed in 18 patients (18/25, 72%) compared to non-tumour sp ...[more]

PMID: 34378327

Similar Datasets

Project description:Abnormal expression of long-noncoding RNA is involved in the tumorigenesis and progression of various cancers, but the potential molecular regulatory mechanisms are unclear. Microbial flora and chronic inflammation, such as periodontitis, which is associated with oral cancer, affect the occurrence and progression of tumors. Accordingly, we stimulated the tongue squamous cell carcinoma (TSCC) cell lines CAL27 and SCC15 with a low concentration of lipopolysaccharide (LPS) from Porphyromonas gingivalis (P.g) for 6 days and then performed LncRNA sequencing on P.g-LPS-treated CAL27 cells and untreated CAL27 cells. LTSCCAT was upregulated in P.g-LPS-treated CAL27 cells compared with untreated CAL27 cells. LTSCCAT induced epithelial-mesenchymal transition and promoted the invasion and metastasis of TSCC in vitro and in vivo. LncRNA LTSCCAT was upregulated in TSCC patients with periodontitis and was correlated with metastasis and poor prognosis. We predicted through an online database and confirmed by dual-luciferase reporter assays that LTSCCAT is a competitive endogenous RNA for the regulation of miR-103a-2-5p. Another dual-luciferase reporter assay confirmed that miR-103a-2-5p has a binding site at the 3'-UTR of the histone methylation transferase SMYD3 and inhibits its translation. Chromatin immunoprecipitation experiments demonstrated that SMYD3 binds directly to the promoter region of TWIST1 and promotes its transcription, which is related to H3K4 trimethylation. The effect of pcDNA/LTSCCAT on expression was attenuated by miR-103a-2-5p mimics. The RF and SVM classifier predicts that LTSCCAT can bind to SMYD3, whereas the RNA immunoprecipitation (RIP) assay confirms that it cannot. In addition, we predicted the combination of LTSCCAT and SMYD3 through software, but the RIP assay confirmed that LTSCCAT could not be combined with SMYD3. For the first time, we showed that periodontitis promotes the invasion and metastasis of TSCC and clarified the molecular mechanism of LTSCCAT to promote invasion and metastasis of TSCC, providing a potential therapeutic target for clinical treatment of TSCC.

Project description:Background Long non-coding ribonucleic acids (lncRNAs) are believed to play crucial roles in cardiovascular diseases; however, details of the underlying mechanisms by which this occurs remain unclear. Methods A mouse heart failure (HF) model was established using isoproterenol (ISO), and confirmed by immunostaining and echocardiography. RNA-sequencing was performed to screen the differential lncRNA expression profiles and heart failure relative lncRNA (HFRL) was selected as the target which was validated by quantitative real-time polymerase chain reaction (qRT-PCR). In HL-1 cells, the cardiac function, inflammatory, and fibrosis-related genes expression changes were examined by qRT-PCR after silencing of HFRL by lentivirus. Meanwhile, Cell Counting Kit-8 (CCK-8) assays were used to detect the effects of HFRL on the cell proliferation and viability. Reactive oxygen species (ROS) assays were also used to explore the role of HFRL in oxidative damage. Next, bioinformatics analysis was conducted to predict the potential binding microRNAs (mmu-miR-149-5p) to HFRL, which was confirmed by RNA-pulldown assays. The target gene of miR-149-5p was also predicted and further validated by Dual-luciferase reporter assays, qRT-PCR, and western blot. To investigate the synergistic regulatory effect of HFRL and miR-149-5p, HL-1 cells were infected with the lentivirus of HFRL with or without simultaneous knockdown of miR-149-5p. Then, qRT-PCR and western blot were used to examine cardiac function, inflammatory, and fibrosis-related gene expression changes, respectively. In HL-1 cells, CCK-8 assays were performed to detect the proliferation and viability. ROS assays were used to explore the oxidative damage. Results The administration of ISO induced mice fibrosis, inflammation, and HF. The in-vitro results showed that knockdown of HFRL suppressed cardiomyocyte proliferation and viability, attenuated inflammatory, cardiac function, and fibrosis-related gene expression, and promoted oxidative damage. HFRL was found to bind to mmu-miR-149-5p and inversely target the 3'-untranscripted region of the collagen 22A1 gene. Thus, HFRL affected cardiomyocyte inflammation, proliferation, viability, oxidative damage, and pro-fibrotic function via sequestration to miR-149-5p. Conclusions The HFRL/miR-149-5p axis plays an important role in regulating cardiac inflammation, proliferation, and fibrosis via a synergistic effect, which suggests that HFRL might be a novel target for HF.

Dataset Information

LncRNA GACAT1 induces tongue squamous cell carcinoma migration and proliferation via miR-149.

Publications

LncRNA GACAT1 induces tongue squamous cell carcinoma migration and proliferation via miR-149.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets