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Background and Aim: Long non‐coding RNA (lncRNA) TNK2 AS1 is a noncoding RNA with the capability of affecting microRNAs (miRNAs) levels and gene expression. The study was designed to investigate the mechanism of TNK2 AS1 in gastric cancer. Methods: The loss and gain of function of TNK2 AS1 were investigated by analyzing the malignant behavior of AGS cells including the abilities of migration, invasion, and epithelial‐mesenchymal transition (EMT) process via wound healing and transwell assay, as well as western blot. The targeting relationship of LncRNA TNK2 AS1 was analyzed through searching bioinformatics database, luciferase reporter assay, and RNA immunoprecipitation (RIP) assay. Tumor‐bearing experiment in nude mice was performed to further confirm the regulatory role of TNK2 AS1 in vivo. Immunofluorescence assay for Ki67 expression was carried out in tumor tissues of mice model. Results: The results showed that TNK2 AS1 overexpression promoted the malignant behaviors of AGS cells, which could be weakened by miR‐125a‐5p mimic addition. In addition, Jumonji, At‐rich interaction domain (JARID2), and phosphatidylinositol 3 kinase (PI3K)/AKT pathway were regulated by TNK2‐AS1/miR‐125a‐5p axis. In vivo, TNK2 AS1/miR‐125a‐5p axis promoted tumor growth and led to increases in green fluorescence intensity and vimentin expression and a decrease in E‐cadherin level, which could be mediated by JARID2 and PI3K/AKT pathway. Conclusion: Therefore, a conclusion was drawn that TNK2‐AS1/miR‐125a‐5p promoted the progression of gastric cancer. [ABSTRACT FROM AUTHOR]

Background: A limited number of studies have reported that the possible effects of coffee intake on skeletal muscle mass, but the results have been inconsistently conclusive and there are no large sample studies concerning the U.S. population. Therefore, the purpose of our study was to explore the connection between coffee consumption and skeletal muscle mass in U.S. adults., Methods: The population for this cross-sectional study was drawn from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018. Appendicular lean mass was accurately obtained from DXA, and skeletal muscle mass was assessed using appendicular skeletal muscle mass adjusted for body mass index (ASMBMI). Coffee and caffeine consumptions were obtained on a 24-h dietary recall questionnaire. Furthermore, the associations between coffee and caffeine intake and skeletal muscle mass were evaluated using three multiple linear regression models and smoothed curve fitting. Subgroup analyses based on age, gender, ethnicity and body mass index (BMI) were performed to assess the robustness of these relationships., Results: This cross-sectional survey included a total of 8,333 participants. After adjusting for all covariates, higher intake of coffee, caffeinated coffee, and caffeine was associated with elevated ASMBMI (coffee: β = 0.01, 95% CI: 0.01, 0.02, P -value < 0.001; caffeinated coffee: β = 0.01, 95% CI: 0.01, 0.02, P -value < 0.001; caffeine: β = 0.02, 95% CI: 0.01, 0.04, P -value < 0.001). Meanwhile, smoothed curve fitting showed that coffee, caffeinated coffee, and caffeine intake were linearly and positively associated with ASMBMI. After further stratification by sex, age, and ethnicity, the positive relationships between coffee (especially caffeinated coffee) and caffeine intake and ASMBMI were not modified ( P for interaction > 0.05). However, these relationships disappeared when the BMI over 30 kg/m 2 ., Conclusions: In general, consumption of coffee and caffeine is positively associated with skeletal muscle mass. Therefore, an appropriate increase in coffee and caffeine intake may be advocated in populations at high risk for low skeletal muscle mass., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yin, Zhu, Guo, Li and Liang.)