LncRNA SLC16A1-AS1 is Upregulated in Glioblastoma and Promotes Cancer Cell Proliferation by Regulating miR-149 Methylation

Abstract

Introduction LncRNA SLC16A1-AS1 has been characterized as a critical player in lung cancer, while its role in glioblastoma (GBM) is unknown. By analyzing the TCGA dataset, we observed the upregulation of SLC16A1-AS1 expression in GBM. Therefore, we aimed to investigate the role of SLC16A1-AS1 in this cancer. Methods GBM tissues and paired non-tumor tissues were collected from 62 GBM patients through biopsy. RT-qPCR was performed to determine the expression of SLC16A1-AS1 and miR-149. Linear regression was used to analyze their correlations. The relationship between SLC16A1-AS1 and miR-149 was assessed by gain and loss of function experiments. Methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) were performed to analyze the methylation status of miR-149. Cell proliferation was evaluated by CCK-8 assay and colony formation experiments in GBM cells. Results We found that SLC16A1-AS1 expression was upregulated in GBM tissues, and the upregulated expression of SLC16A1-AS1 predicted poor survival of GBM patients. MiR-149 was downregulated in GBM tissues and inversely correlated with the expression of SLC16A1-AS1. In GBM cells, overexpression of SLC16A1-AS1 downregulated the expression of miR-149 and increased the methylation of miR-149 gene. In cell proliferation and colony formation assay, overexpression of SLC16A1-AS1 reduced the inhibitory effects of miR-149 on GBM cell proliferation. Conclusion SLC16A1-AS1 may promote GBM cell proliferation by regulating miR-149 methylation. SLC16A1-AS1 can be considered as a potential diagnostic marker in GBM.

Monocarboxylate Transporters are Involved in Extracellular Matrix Remodelling in Pancreatic Ductal Adenocarcinoma

“…Hence it is important to understand and correlate expression of MCTs and ECMs in different compartments. Our analysis revealed nine differentially expressed MCT genes in both stromal and epithelial samples including the upregulated thyroid hormone (TH) transporters MCT8 (SLC16A12) and MCT10 (SLC16A10), monocarboxylate transporter MCT2 (SLC16A7), MCT6 (SLC16A5) with potential role in glucose and lipid metabolism, and an lncRNA SLC16A1-AS1 previously identified as a prognostic or diagnostic biomarker in a number of cancers [13,[47][48][49][50][51][52][53][54]. To our knowledge, the upregulation of the TH transporters in the stromal-epithelial samples has not been highlighted previously.…”

“…Therefore, better understanding of the molecular mechanisms involved in contribution of THs to pancreatic cancer is needed. The lncRNA SLC16A1-AS1 has previously been found to be upregulated in osteosarcoma, glioblastoma and oral squamous cell carcinoma [50, 52, 63], downregulated in non-small cell lung cancer and cervical squamous cell carcinoma [19, 49], and show conflicting expression profile in hepatocellular carcinoma [51, 53, 54]. This is the first study highlighting differential expression of SLC16A1-AS1 in PDAC showing lower levels of expression in epithelial relative to stromal compartment.…”

Monocarboxylate Transporters Are Involved in Extracellular Matrix Remodelling in Pancreatic Ductal Adenocarcinoma

“…Hence, it is important to understand and correlate the expression of MCTs and ECMs in different compartments. Our analysis revealed nine differentially expressed MCT genes in both stromal and epithelial samples, including the upregulated thyroid hormone (TH) transporters MCT8 ( SLC16A12 ) and MCT10 ( SLC16A10 ), monocarboxylate transporter MCT2 ( SLC16A7 ), MCT6 ( SLC16A5 ) with a potential role in glucose and lipid metabolism, and an lncRNA SLC16A1-AS1 previously identified as a prognostic or diagnostic biomarker in a number of cancers [ 20 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 ]. To our knowledge, the upregulation of the TH transporters in the stromal–epithelial samples has not been highlighted previously.…”

Upregulation of 15 Antisense Long Non-Coding RNAs in Osteosarcoma

“…The upregulation of SLC16A1-AS1 was observed in hepatocellular carcinoma, and glioblastoma [67,68]. Hong Yue Liu et al suggested that the transcript was dramatically downregulated in non-small cell lung cancer and over expression of SLC16A1-AS1 inhibits the cell viability and proliferation of lung cancer cell [69].…”