Clinical efficacy and mechanism study of mid-frequency anti-snoring device in treating moderate obstructive sleep apnea-hypopnea syndrome.

BACKGROUND: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is primarily caused by airway obstruction due to narrowing and blockage in the nasal and nasopharyngeal, oropharyngeal, soft palate, and tongue base areas. The mid-frequency anti-snoring device is a new technology based on sublingual nerve stimulation. Its principle is to improve the degree of oropharyngeal airway stenosis in OSAHS patients under mid-frequency wave stimulation. Nevertheless, there is a lack of clinical application and imaging evidence. AIM: To investigate the clinical efficacy and mechanisms of a mid-frequency anti-snoring device in treating moderate OSAHS. METHODS: We selected 50 patients diagnosed with moderate OSAHS in our hospital between July 2022 and August 2023. They underwent a 4-wk treatment regimen involving the mid-frequency anti-snoring device during nighttime sleep. Following the treatment, we monitored and assessed the sleep apnea quality of life index and Epworth Sleepiness Scale scores. Additionally, we performed computed tomography scans of the oropharynx in the awake state, during snoring, and while using the mid-frequency anti-snoring device. Cross-sectional area measurements in different states were taken at the narrowest airway point in the soft palate posterior and retrolingual areas. RESULTS: Compared to pretreatment measurements, patients exhibited a significant reduction in the apnea-hypopnea index, the percentage of time with oxygen saturation below 90%, snoring frequency, and the duration of the most prolonged apnea event. The lowest oxygen saturation showed a notable increase, and both sleep apnea quality of life index and Epworth Sleepiness Scale scores improved. Oropharyngeal computed tomography scans revealed that in OSAHS patients cross-sectional areas of the oropharyngeal airway in the soft palate posterior area and retrolingual area decreased during snoring compared to the awake state. Conversely, during mid-frequency anti-snoring device treatment, these areas increased compared to snoring. CONCLUSION: The mid-frequency anti-snoring device demonstrates the potential to enhance various sleep parameters in patients with moderate OSAHS, thereby improving their quality of life and reducing daytime sleepiness. These therapeutic effects are attributed to the device's ability to ameliorate the narrowing of the oropharynx in OSAHS patients.

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer.

Abnormal angiogenesis is a critical factor in tumor growth and metastasis, and protein arginine methyltransferase 5 (PRMT5), a prominent type II enzyme, is implicated in various human cancers. However, the precise role of PRMT5 in regulating angiogenesis to promote lung cancer cell metastasis and the underlying molecular mechanisms are not fully understood. Here, we show that PRMT5 is overexpressed in lung cancer cells and tissues, and its expression is triggered by hypoxia. Moreover, inhibiting or silencing PRMT5 disrupts the phosphorylation of the VEGFR/Akt/eNOS angiogenic signaling pathway, NOS activity, and NO production. Additionally, inhibiting PRMT5 activity reduces HIF-1α expression and stability, resulting in the down-regulation of the VEGF/VEGFR signaling pathway. Our findings indicate that PRMT5 promotes lung cancer epithelial-mesenchymal transition (EMT), which might be possibly through controlling the HIF-1α/VEGFR/Akt/eNOS signaling axis. Our study provides compelling evidence of the close association between PRMT5 and angiogenesis/EMT and highlights the potential of targeting PRMT5 activity as a promising therapeutic approach for treating lung cancer with abnormal angiogenesis.

PRMT5/FGFR3/AKT Signaling Axis Facilitates Lung Cancer Cell Metastasis.

Objectives: This study aims to investigate the function of the protein arginine methyltransferase 5 (PRMT5) and fibroblast growth factor receptor 3 (FGFR3)/Akt signaling axis in the epithelial-mesenchymal transition (EMT) of human lung cancer. Methods: The mRNA and protein expression levels of PRMT5, FGFR3, p-Akt, and EMT markers are determined by quantitative real-time PCR and Western blotting, respectively; the expression and localization of PRMT5, p-Akt, and proliferating cell nuclear antigen are detected by immunofluorescence; the human lung cancer cell proliferation is measured by MTS assay. Results: PRMT5 and FGFR3 are highly expressed in human lung cancer tissues and are closely related to lymphatic metastasis. Moreover, down-regulation of PRMT5 by lentivirus-mediated shRNAs or inhibition of PRMT5 by specific inhibitors attenuates FGFR3 expression, Akt phosphorylation, and lung cancer cell proliferation. Further studies show that silencing PRMT5 impairs EMT-related markers, including vimentin, collagen I, and ß-catenin. Conversely, ectopic expression of PRMT5 increases FGFR3 expression, Akt phosphorylation, and EMT-related markers, suggesting that PRMT5 regulates metastasis probably through the FGFR3/Akt signaling axis. Conclusion: PRMT5/FGFR3/Akt signaling axis controls human lung cancer progression and metastasis and also implies that PRMT5 may serve as a prognostic biomarker and therapeutic candidate for treating lung cancer.