METHODS: miR-3191 expression is determined via quantitative real-time polymerase chain reaction. Knockdown and overexpression of miR-3191 influence the proliferation and metastasis of HCC cells, which is measured by Cell Counting Kit-8 assay, Colony Formation assay and Cell metastasis assay. Protein expression is estimated by Western blot. The interplay between miR-3191 and target is validated by dual-luciferase reporter assay.
RESULTS: Here, we show that miR-3191 is upregulated in HCC tissues and associated with poor prognosis of HCC patients. Mechanistically, p21-activated protein kinase 6 (PAK6) was identified as a direct target of miR‑3191 in HCC. PAK6 knockdown partially recovered interference of miR‑3191‑induced decrease in cell proliferation and invasion. The accuracy of HCC patient prognosis could be improved by employing a combination of miR-3191 and PAK6 values.
CONCLUSIONS: miR-3191 promotes the proliferation and metastasis of HCC cells via targeting PAK6 and may serve as a prognostic biomarker and potential therapeutic target.
METHODS: We conducted a comprehensive search on March 15, 2024, using Web of Science, PubMed, Scopus, and EBSCOhost. Eligibility criteria for selecting studies were established based on the PICOS framework: (i) Population-healthy soccer players; (ii) Intervention-SAQ training; (iii) Comparison condition (conventional training or traditional training); (iv) Outcome-physical performance (speed, agility, strength, etc.); (v) Study design-randomized controlled trials. The PEDro scale was employed to evaluate the methodological quality of each study, and a random-effects model was used for the meta-analysis.
RESULTS: A total of 11 studies met the inclusion criteria for the systematic literature review. One study with low PEDro score was excluded, and one was excluded based on Cochrane bias risk assessment. Finally, 9 studies were included in the meta-analysis, comprising 498 soccer players. Overall, the results indicated a significant impact of SAQ training on physical qualities and dribbling speed among soccer players. Specifically, there was a moderate effect size for sprint performance (5m, 10m, 20m) (ES = 0.75; p < 0.01), change of direction ability (COD) (ES = 0.35; p < 0.001), power (vertical and horizontal jumps) (ES = 0.67; p < 0.01), while flexibility showed no significant impact (ES = 0.11; p > 0.05). Moreover, change-of-direction dribbling demonstrated a significant effect (ES = 0.58; p < 0.01).
CONCLUSION: Overall, SAQ training effectively enhances speed, COD, explosiveness, and change-of-direction dribbling specific performance in adolescent soccer players, particularly in sprinting. However, it does not have an advantage in improving flexibility. Further high-quality studies encompassing a broader range of exercises are needed to fully determine the effectiveness of SAQ training in improving other physical qualities and technical skills of soccer players, as well as ultimately enhancing match performance.
METHODS: Reverse-transcription-polymerase chain reaction was employed to measure the expression of plasmacytoma variant translocation 1 (PVT1), microRNAs (miRNAs), and SIRT3, and the dual-luciferase assay was used to determine their interaction. Electron microscopy observes autophagosomes, green fluorescent protein-microtubule-associated protein 1 light chain 3 (GFP-LC3) staining, and immunoblot analysis with antibodies against LC3，beclin-1, and P62 were conducted to measure autophagy. Cellular senescence was determined using immunoblot analysis with anti-phosphorylated retinoblastoma and senescence-associated β-galactosidase staining.
RESULTS: Women with higher estrogen levels (during the 10-13th day of the menstrual cycle or premenopausal) exhibit markedly higher serum levels of PVT1 than women with lower estrogen levels (during the menstrual period or postmenopausal). The dual-luciferase assay showed that PVT1 acts as a sponge for miR-31, and miR-31 binds to its target gene, SIRT3. The 17β-E2 treatment increased the expression of PVT1 and SIRT3 and downregulated miR-31 expression in human umbilical vein endothelial cells (HUVECs). Consistently, PVT1 overexpression suppresses miR-31 expression, promotes 17β-E2-induced autophagy, and inhibits H2O2-induced senescence. miR-31 inhibitor increases SIRT3 expression and leads to activation of 17β-E2-induced autophagy and suppression of H2O2-induced senescence.
CONCLUSION: Our findings demonstrated that 17β-E2 upregulates PVT1 gene expression and PVT1 functions as a sponge to inhibit miR-31, resulting in the upregulation of SIRT3 expression and activation of autophagy and subsequent inhibition of H2O2-induced senescence in HUVECs.