Expression and relevant bioinformatics analysis of miR-135b-5p in oral squamous cell carcinoma / 口腔疾病防治

Objective @# To observe the clinical significance of miR-135b-5p in oral squamous cell carcinoma (OSCC) tissues and to conduct a bioinformatics analysis of its predicted target genes.@*Methods @#The expression levels of miR-135b-5p in OSCC tissues and adjacent normal tissues were compared using data from TCGA and GEO databases, and the correlations of miR-135b-5p expression level with clinicopathologic characteristics were analyzed. Fresh tissues were collected in the clinic, and the expression of miR-135b-5p was verified by quantitative real-time PCR. The target genes with enriched pathways were analyzed by using bioinformatics methods. A protein-protein interaction network was constructed to screen hub genes.@*Results @#The expression levels of miR-135b-5p were significantly upregulated in OSCC tissues compared to adjacent normal tissues (P < 0.001) and had a good diagnostic capability (AUC=0.960, P < 0.001). The expression level of miR-135b-5p was positively correlated with histopathological grading (P=0.011). Enrichment analyses revealed that the target genes of miR-135b-5p were significantly associated with tumor-related signaling pathways, such as the calcium signaling pathway, the cGMP-PKG signaling pathway and the cAMP signaling pathway. Ten core target genes were obtained by screening: DLG2, ANK3, ERBB4, SCN2B, NBEA, GABRB2, ATP2B2, SNTA1, CACNA1D, and SPTBN4.@*Conclusion@#miR-135b-5p may act as an oncogene miRNA in OSCC and has the potential value of acting as a diagnostic biomarker and therapeutic target for OSCC.

CircRNA RSF1 regulated ox-LDL induced vascular endothelial cells proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in atherosclerosis

BACKGROUND: Atherosclerosis (AS) is the most common type in cardiovascular disease. Due to its complex pathogenesis, the exact etiology of AS is unclear. circRNA has been shown to play an essential role in most diseases. However, the underlying mechanism of circRNA in AS has been not understood clearly. METHODS: Quantitative Real-Time PCR assay was used to detect the expression of circRSF1, miR-135b-5p and histone deacetylase 1 (HDAC1). Western blot was applied to the measure of protein expression of HDAC1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cleaved-caspase-3, vascular cell adhesion molecule 1 (VCAM1), intercellular cell adhesion molecule-1 (ICAM1) and E-selectin. MTT assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter assay and RIP assay was used to determine the relationship among circRSF1, miR-135b-5p and HDAC1. Besides, an ELISA assay was performed to measure the levels of IL-1ß, IL-6, TNF-α and IL-8. RESULTS: In this study, ox-LDL inhibited circRSF1 and HDAC1 expression while upregulated miR-135b-5p expression in Human umbilical vein endothelial cells (HUVECs). Importantly, ox-LDL could inhibit HUVECs growth. Moreover, promotion of circRSF1 or inhibition of miR-135b-5p induced cell proliferation while inhibited apoptosis and inflammation of ox-LDL-treated HUVECs, which was reversed by upregulating miR-135b-5p or downregulating HDCA1 in oxLDL-treated HUVECs. More than that, we verified that circRSF1 directly targeted miR-135b-5p and HDAC1 was a target mRNA of miR-135b-5p in HUVECs. CONCLUSION: CircRSF1 regulated ox-LDL-induced vascular endothelial cell proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in AS, providing new perspectives and methods for the treatment and diagnosis of AS.

Long non-coding RNA MALAT1 regulates cell proliferation and apoptosis via miR-135b-5p/GPNMB axis in Parkinson's disease cell model

BACKGROUNDS: Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. METHODS: SK-N-SH and SK-N-BE cells were treated with MPP+ to establish the MPP+-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP+-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP+-stimulated cell model of PD were explored. RESULTS: MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. CONCLUSION: Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP+-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.