Dataset Information

Long Non-Coding RNA SLC25A21-AS1 Promotes Multidrug Resistance in Nasopharyngeal Carcinoma by Regulating miR-324-3p/IL-6 Axis.

ABSTRACT:

Background

Nasopharyngeal carcinoma (NPC), one of the most common types of head and neck tumor, occurred in the epithelial lining of the nasopharynx and is mainly prevalent in Southeast Asia and Southern China. However, the molecular mechanisms of NPC multidrug resistance still remained largely unclear.

Methods

The qRT-PCR assay was performed to examine SLC25A21-AS1, miR-324-3p and IL-6 expression in NPC tissues and cell. The CCK8 assay and colony formation assay were used to detect cell growth. In addition, CCK8 assay was performed to detect IC₅₀ values of different drugs in NPC cell.

Results

In this study, we found that SLC25A21-AS1 expression was increased in NPC tissues and cell line, and knockdown of SLC25A21-AS1 inhibited cell growth and MDR in NPC cell. Moreover, SLC25A21-AS1 acted as a ceRNA for miR-324-3p and facilitates NPC cell growth and MDR by regulating the miR-324-3p/IL-6 axis.

Conclusion

Our findings demonstrated the role of SLC25A21-AS1/miR-324-3p/IL-6 axis in cell growth and MDR in NPC, which might be a potential prognostic and diagnostic marker in NPC patients and provide new insight into the molecular mechanism of MDR in NPC chemotherapy.

SUBMITTER: Wang X

PROVIDER: S-EPMC7264158 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

Long Non-Coding RNA SLC25A21-AS1 Promotes Multidrug Resistance in Nasopharyngeal Carcinoma by Regulating miR-324-3p/IL-6 Axis.

Wang Xiaoqin X Wang Chunhui C Xu Hong H Xie Hong H

Cancer management and research 20200526

<h4>Background</h4>Nasopharyngeal carcinoma (NPC), one of the most common types of head and neck tumor, occurred in the epithelial lining of the nasopharynx and is mainly prevalent in Southeast Asia and Southern China. However, the molecular mechanisms of NPC multidrug resistance still remained largely unclear.<h4>Methods</h4>The qRT-PCR assay was performed to examine SLC25A21-AS1, miR-324-3p and IL-6 expression in NPC tissues and cell. The CCK8 assay and colony formation assay were used to dete ...[more]

PMID: 32547230

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Project description:BackgroundObesity alters metabolic microenvironment and is thus associated with several tumours. The aim of the present study was to investigate the role, molecular mechanism of action, and potential clinical value of lipid metabolism-related long non-coding RNA (lncRNA) SLC25A21-AS1 in oesophageal squamous cell carcinoma (ESCC).MethodsA high-fat diets (HFDs)-induced obesity nude mouse model was established, and targeted metabolomics analysis was used to identify critical medium-long chain fatty acids influencing the growth of ESCC cells. Transcriptomic analysis of public dataset GSE53625 confirmed that lncRNA SLC25A21-AS1 was a lipid metabolism-related lncRNA. The biological function of lncRNA SLC25A21-AS1 in ESCC was investigated both in vivo and in vitro. Chromatin immunoprecipitation(ChIP)assay, RNA-pull down, mass spectrometry, co-IP, and RNA IP(RIP) were performed to explore the molecular mechanism. Finally, an ESCC cDNA microarray was used to determine the clinical prognostic value of SLC25A21-AS1 by RT-qPCR.ResultsPalmitic acid (PA) is an important fatty acid component of HFD and had an inhibitory effect on ESCC cell lines. LncRNA SLC25A21-AS1 expression was downregulated by PA and associated with the proliferation and migration of ESCC cells in vitro and in vivo. Mechanistically, SLC25A21-AS1 interacted with nucleophosmin-1 (NPM1) protein to promote the downstream gene transcription of the c-Myc in the nucleus. In the cytoplasm, SLC25A21-AS1 maintained the stability of SLC25A21 mRNA and reduced the intracellular NAD+ /NADH ratio by influencing tryptophan catabolism. Finally, we demonstrated that high expression of SLC25A21-AS1 promoted resistance to cisplatin-induced apoptosis and was correlated with poor tumour grade and overall survival.ConclusionsHFD/PA has an inhibitory effect on ESCC cells and SLC25A21-AS1 expression. SLC25A21-AS1 promotes the proliferation and migration of ESCC cells by regulating the NPM1/c-Myc axis and SLC25A21 expression. In addition, lncRNA SLC25A21-AS1 may serve as a favourable prognostic biomarker and a potential therapeutic target for ESCC.

Project description:BackgroundThe venous malformation is the most common congenital vascular malformation and exhibits the characteristics of local invasion and lifelong progressive development. Long noncoding RNA (lncRNA) regulates endothelial cells, vascular smooth muscle cells, macrophages, vascular inflammation, and metabolism and also affects the development of venous malformations. This study aimed to elucidate the role of the lncRNA LEF1-AS1 in the development of venous malformations and examine the interaction among LEF1-AS1, miR-489-3p, and S100A11 in HUVEC cells.MethodsVenous malformation tissues, corresponding normal venous tissues, and HUVEC cells were used. Agilent human lncRNA microarray gene chip was used to screen differential genes, RNA expression was detected using quantitative reverse transcription PCR, and protein expression was detected using Western blotting. The proliferation, migration, and angiogenesis of HUVEC cells were assessed using CCK8, transwell, and in vitro angiogenesis tests.ResultsA total of 1,651 lncRNAs were screened using gene chip analysis, of which 1015 were upregulated and 636 were downregulated. The lncRNA LEF1-AS1 was upregulated with an obvious difference multiple, and the fold-change value was 11.03273. The results of the analysis performed using the StarBase bioinformatics prediction website showed that LEF1-AS1 and miR-489-3p possessed complementary binding sites and that miR-489-3p and S100A11 also had complementary binding sites. The findings of tissue experiments revealed that the expressions of LEF1-AS1 and S100A11 were higher in tissues with venous malformations than in normal tissues, whereas the expression of miR-489-3p was lower in venous malformations than in normal tissues. Cell culture experiments indicated that LEF1-AS1 promoted the proliferation, migration, and angiogenesis of HUVEC cells. In these cells, LEF1-AS1 targeted miR-489-3p, which in turn targeted S100A11. LEF1-AS1 acted as a competitive endogenous RNA and promoted the expression of S100A11 by competitively binding to miR-489-3p and enhancing the proliferation, migration, and angiogenesis of HUVEC cells. Thus, LEF1-AS1 participated in the occurrence and development of venous malformation.ConclusionsThe expression of LEF1-AS1 was upregulated in venous malformations, and the expression of S100A11 was increased by the adsorption of miR-489-3p to venous endothelial cells, thus enhancing the proliferation, migration, and angiogenesis of HUVEC cells. In conclusion, LEF1-AS1 is involved in the occurrence and development of venous malformations by regulating the miR-489-3p/S100A11 axis, which provides valuable insights into the pathogenesis of this disease and opens new avenues for its treatment.

Dataset Information

Long Non-Coding RNA SLC25A21-AS1 Promotes Multidrug Resistance in Nasopharyngeal Carcinoma by Regulating miR-324-3p/IL-6 Axis.

Background

Methods

Results

Conclusion

Publications

Long Non-Coding RNA SLC25A21-AS1 Promotes Multidrug Resistance in Nasopharyngeal Carcinoma by Regulating miR-324-3p/IL-6 Axis.

Similar Datasets

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