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Background Gastric cancer (GC) is one of the most severe cancers worldwide, particularly in China. Circular RNA (circRNA) plays an essential role in GC. Hsa_circ_0000285 regulates the progression of several cancers. However, its role in GC has not been reported. This study elucidated the molecular mechanism and role of hsa_circ_0000285 in GC progression. Methods GC cells were transfected with silencers of hsa_circ_0000285 and fibronectin 1 ( FN1 ), an inhibitor of miR‐1278, and their negative controls (NC). Mice were injected with short hairpin (sh) RNAs targeting hsa_circ_0000285 or NC. The expression levels of hsa_circ_0000285 , miR‐1278, and FN1 were assessed using western blotting and reverse transcription quantitative real‐time polymerase chain reaction (qRT‐PCR). Several assays were used to evaluate cell proliferation, invasion, and apoptosis. Tumor burden was also analyzed. The interactions between miR‐1278, hsa_circ_0000285 , and FN1 were ascertained using dual‐luciferase reporter assays. An RNA immunoprecipitation (RIP) assay was used to assess the enrichment of hsa_circ_0000285 and miR‐1278 in GC. Results Hsa_circ_0000285 was significantly overexpressed in the GC tissues. Silencing hsa_circ_0000285 inhibited cell proliferation and invasion, promoted apoptosis, and inhibited tumor development. Hsa_circ_0000285 sponged miR‐1278. Inhibition of miR‐1278 in vitro reversed the effects of hsa_circ_0000285 silencing on GC progression. MiR‐1278 targeted FN1 , and silencing FN1 neutralized the effects of miR‐1278 inhibitors on GC progression. Conclusions The hsa_circ_0000285 /miR‐1278/ FN1 axis regulated GC progression. In addition, it may serve as a potential therapeutic biomarker for GC.

Menopausal hormone therapy (MHT) was widely used to treat menopause-related symptoms in menopausal women. However, MHT therapies were controversial with the increased risk of breast cancer because of different estrogen and progestogen combinations, and the molecular basis behind this phenomenon is currently not understood. To address this issue, we identified differentially expressed genes (DEGs) between the estrogen plus progestogens treatment (EPT) and estrogen treatment (ET) using the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data. As a result, a total of 96 upregulated DEGs were first identified. Seven DEGs related to the cell cycle (CCNE2, CDCA5, RAD51, TCF19, KNTC1, MCM10, and NEIL3) were validated by RT-qPCR. Specifically, these seven DEGs were increased in EPT compared to ET (p < 0.05) and had higher expression levels in breast cancer than adjacent normal tissues (p < 0.05). Next, we found that estrogen receptor (ER)-positive breast cancer patients with a higher CNNE2 expression have a shorter overall survival time (p < 0.05), while this effect was not observed in the other six DEGs (p > 0.05). Interestingly, the molecular docking results showed that CCNE2 might bind to 17β-estradiol (−6.791 kcal/mol), progesterone (−6.847 kcal/mol), and medroxyprogesterone acetate (−6.314 kcal/mol) with a relatively strong binding affinity, respectively. Importantly, CNNE2 protein level could be upregulated with EPT and attenuated by estrogen receptor antagonist, acolbifene and had interactions with cancer driver genes (AKT1 and KRAS) and high mutation frequency gene (TP53 and PTEN) in breast cancer patients. In conclusion, the current study showed that CCNE2, CDCA5, RAD51, TCF19, KNTC1, MCM10, and NEIL3 might contribute to EPT-related tumorigenesis in breast cancer, with CCNE2 might be a sensitive risk indicator of breast cancer risk in women using MHT.

ObjectiveThe prevalence of stress urinary incontinence (SUI) increases around menopause. The quality of life of perimenopausal and postmenopausal women with SUI is significantly affected. This study aimed to investigate the prevalence of SUI and the associated risk factors in a population of Chinese perimenopausal and postmenopausal women.MethodsA total of 273 perimenopausal and postmenopausal women were enrolled, and a cross‐sectional study was conducted. SUI was defined as an involuntary loss of urine with increases in abdominal pressure. Data including personal characteristics, menopause information, estrogen levels, and pelvic floor muscle strength levels were statistically analyzed.ResultsThe study enrolled 158 (57.9%) perimenopausal and 115 (42.1%) postmenopausal women. Sixty‐six (41.8%) perimenopausal women and 56 (48.7%) postmenopausal women complained of SUI. The mean age was 49.42 ± 5.58 years. Body mass index over 24 kg/m2 (odds ratio [OR] 2.02, 95% confidence interval [CI] 1.07–3.81), vaginal delivery (OR 2.47, 95% CI 1.33–4.58), and diabetes (OR 4.65, 95% CI 1.23–17.62) were high‐risk factors for SUI. Climacteric symptoms (evaluated by Kupperman index scores) were statistically related to SUI, and among the 13 symptoms, insomnia, nervousness, weakness and fatigue, arthralgia and myalgia, headache, palpitation, and sexual complaints were all correlated with SUI in perimenopausal and postmenopausal women.ConclusionsSeveral factors are associated with SUI in Chinese perimenopausal and postmenopausal women. Obesity, vaginal delivery, climacteric symptoms, and diabetes were identified as the most notable risk factors. The management strategy could focus on the prevention and management of risk factors.