Efficacy of continuous positive airway pressure on TNF-α in obstructive sleep apnea patients: A meta-analysis.

BACKGROUND: Tumor necrosis factor-α (TNF-α) is an important mediator of the immune response. At present, the improvement of TNF-α after continuous positive airway pressure (CPAP) treatment of obstructive sleep apnea-hypopnea syndrome (OSAHS) is still controversial. METHODS: We conducted a systematic review of the present evidence based on a meta-analysis to elucidate the effects of TNF-α on OSAHS after CPAP treatment. RESULTS: To measure TNF-α, ten studies used enzyme-linked immunosorbent assay (ELISA), and one used radioimmunoassay. The forest plot outcome indicated that CPAP therapy would lower the TNF-α levels in OSAHS patients, with a weighted mean difference (WMD) of 1.08 (95% CI: 0.62-1.55; P < 0.001) based on the REM since there is highly significant heterogeneity (I2 = 90%) among the studies. Therefore, we used the subgroup and sensitivity analyses to investigate the source of heterogeneity. The findings of the sensitivity analysis revealed that the pooled WMD ranged from 0.91 (95% CI: 0.52-1.31; P < 0.001) to 1.18 (95% CI: 0.74-1.63; P < 0.001). The findings were not influenced by any single study. Notably, there was homogeneity in the Asia subgroup and publication year: 2019, implying that these subgroups could be the source of heterogeneity. CONCLUSION: Our meta-analysis recommends that CPAP therapy will decrease the TNF-α level in OSAHS patients, but more related research should be conducted.

CircPTPRM accelerates malignancy of papillary thyroid cancer via miR-885-5p/DNMT3A axis.

BACKGROUND: Circular RNAs (circRNAs) are implicated in carcinogenesis, including papillary thyroid cancer (PTC). Despite of previous reports regarding the high expression of circPTPRM in PTC, the role and regulatory mechanism remain to be investigated. METHODS: CircPTPRM and miR-885-5p expression were examined, and the effects on cell proliferation, migration, and invasion were also measured. Immunoblotting was performed to evaluate DNA methyltransferase 3A (DNMT3A) and the epithelial-mesenchymal transition (EMT)-associated proteins. RESULTS: CircPTPRM was overexpressed in PTC tissues and cell lines, which predicted poor prognosis. CircPTPRM inhibition significantly alleviated the proliferation, migration, and invasion abilities. It was subsequently confirmed that circPTPRM competed with miR-885-5p for DNMT3A binding. CircPTPRM promoted PTC progression via miR-885-5p/DNMT3A signal axis. CONCLUSION: Our data elucidated that circPTPRM may play an oncogenic role in PTC through circPTPRM/miR-885-5p/DNMT3A axis.

Circ_0005033 is an oncogene in laryngeal squamous cell carcinoma and regulates cell progression and Cisplatin sensitivity via miR-107/IGF1R axis.

Transcriptome expression profiles of laryngeal squamous cell carcinoma (LSCC) are altered, and we aimed to investigate expression and role of hsa_circ_0005033 (circ_0005033), microRNA (miR)-107 and insulin-like growth factor 1 receptor (IGF1R) in LSCC. Real-time PCR, western blotting and immunohistochemistry detected RNA and protein expression levels. Functional assays were performed using MTT assay, EdU assay, apoptosis assay, flow cytometry, Transwell assay, and xenograft tumor model. Direct interaction was predicted by Starbase algorithm and validated by dual-luciferase reporter assay and RNA immunoprecipitation. Expression of circ_0005033 was substantially upregulated in LSCC tissues and cells, and allied with miR-107 downregulation and IGF1R upregulation. Circ_0005033 showed a closed-loop structure and long half-life. Essentially, circ_0005033 and IGF1R were competing endogenous RNAs for miR-107 via target binding. Silencing circ_0005033 facilitated apoptosis rate and lowered cell viability, proliferation, migration and invasion of LSCC cells, as well as delayed xenograft tumor growth. Allied with that, cleaved-caspase 3/8/9 expression was elevated via death receptor-mediated and mitochondrial pathways, and expression of matrix metalloproteinase-2 (MMP2), MMP9, cyclin D1 and proliferating cell nuclear antigen was decreased. Moreover, Cisplatin-induced inhibition of cell viability was exacerbated by inhibiting circ_0005033. These functional effects of circ_0005033 depression were consistent with those of miR-107 overexpression. Furthermore, depleting miR-107 and restoring IGF1R abated the effects of circ_0005033 knockdown and miR-107 overexpression, respectively. Circ_0005033 was oncogenic in LSCC by regulating cell progression and Cisplatin sensitivity at least via miR-107/IGF1R axis.