Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. Several clinical trials have investigated the influence of carnitine on metabolic variables in PCOS, but have yielded conflicting results. This study aimed to summarize the clinical evidence of the effects of carnitine on weight management, glycemic and serum lipids controls in women with PCOS by conducting a meta-analysis of randomized control trials (RCTs). PubMed, Embase, Web of Sciences, Scopus, and the CENTRAL database were searched from inception to March 2021 for eligible articles. Study selection and assessment of quality were conducted independently by two investigators. Effect sizes for each outcome were reported with the weighted mean differences (WMDs) and 95% confidence intervals (CIs). The statistical heterogeneity of the included clinical trials was tested using the I2 statistic. Six studies with 672 PCOS participants were included for meta-analysis. Our results revealed that carnitine supplements significantly decreased total cholesterol, low-density lipoprotein-cholesterol, triglycerides, body weight, body mass index, hip circumference, and waist circumference (All p < .05). In addition, carnitine intervention also improved the levels of high-density lipoprotein cholesterol. However, no significant changes were seen in glucose homeostasis parameters. These results were stable after sensitivity analysis, and no significant publication biases were detected. Based on current evidence, carnitine supplementation in women with PCOS had beneficial effects on weight loss and lipid profiles. Further large-scale, well-designed RCTs are required to confirm these results.
Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been unraveled to exert regulatory effects on cancer progression, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p/Forkhead box K2 (FOXK2) axis remains rarely explored. This study aims to unearth the regulatory mechanism of TP53TG1/miR-33a-5p/FOXK2 axis in CC. The CC clinical samples were collected, and CC cells were cultured. TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues and cells. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 or miR-33a-5p to determine the changes of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. TP53TG1 and FOXK2 expression levels were increased and miR-33a-5p expression level was reduced in CC cells and tissues. The silenced TP53TG1 or FOXK2, or elevated miR-33a-5p decelerated the CC cell development and restrained the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or elevated miR-33a-5p reversed the effects of decreased TP53TG1 on CC cell progression. TP53TG1 sponged miR-33a-5p, which targeted FOXK2. The experiment in vivo validated the outcomes of the experiment in vitro. TP53TG1 accelerates the CC development via regulating miR-33a-5p to target FOXK2 with the involvement of PI3K/AKT/mTOR signaling pathway. This study provides novel theory basis and distinct therapeutic targets for CC treatment.
Cervical cancer (CC) is the fourth most prevalent type of cancer in women worldwide and it is considered the leading cause of tumor-related death and malignancy. As part of complexes involved in epigenetic control, the proteins of the chromobox (CBX) family have been found to have a role in the growth of malignancies by preventing differentiation and increasing proliferation. Here, by a thorough investigation, we investigated the expression, prognostic significance, and immune infiltration of CBX in patients with CC.Differential expression, clinicopathological parameters, immune cell infiltration, enrichment analysis, genetic alteration, and prognostic value of CBXs in patients with CC were examined using TIMER, Metascape, STRING, GeneMANIA, cBioPortal, UALCAN, The Human Protein Atlas, Gene Expression Profiling Interactive Analysis (GEPIA), and Oncomine.In CC tissues, CBX 2/3/4/5 and CBX 8 expression levels were considerably higher, whereas CBX 6/7 expression levels were lower. In CC, the CBX 5/6/8 promoters have elevated levels of methylation. The expression of CBX 2/6/8 and the pathological stage were connected. A 37% mutation rate of the differentially expressed CBX genes was observed. Also, there was a strong correlation of the CBXs expression with immune cell infiltration, such as T CD4+ cells, macrophages, neutrophils, B cells, T CD8+ cells, and dendritic cells.The investigation discovered that members of the CBXs family may be therapeutic targets for CC patients and may play significant roles in the development of CC tumors.
BACKGROUND Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been studied in multiple diseases, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p to target Forkhead box K2 (FOXK2) remains limited. This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. OBJECTIVE This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. METHODS The clinical samples were collected and TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 and miR-33a-5p to determine the change of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. RESULTS TP53TG1 and FOXK2 were enriched and miR-33a-5p was inhibited in CC. The reduced TP53TG1 or FOXK2 or elevated miR-33a-5p decelerated the CC cell development and the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or enriched miR-33a-5p reversed the effects of decreased TP53TG1. TP53TG1 sponged miR-33a-5p which targeted FOXK2. The experiment in vivo validated the outcomes of the experiment in vitro. CONCLUSIONS TP53TG1 accelerates the CC development via regulating miR-33a-5p to target FOXK2 with the involvement of PI3K/AKT/mTOR signaling pathway. This study provides novel theory references and a distinct direction for the therapy strategies of CC.
Many studies proposed that cytochrome P450 1A1 (CYP1A1) MspI polymorphism may be associated with endometrial cancer risk, but the findings from previous studies reported conflicting results. A meta-analysis of all relevant studies was performed to get a comprehensive assessment of the association between CYP1A1 MspI polymorphism and endometrial cancer risk. Eligible studies were searched in PubMed and China National Knowledge Infrastructure databases. The pooled odds ratios (ORs) with the corresponding 95 % confidence intervals (95 % CIs) were calculated to evaluate the association. Twelve studies with a total of 2,111 cases and 2,894 controls were finally included into the meta-analysis. Overall, meta-analysis of a total of 12 studies showed that there was no obvious association between CYP1A1 MspI polymorphism and endometrial cancer risk (ORC vs. T = 0.97, 95 % CI 0.77-1.22, P OR = 0.808; ORCC vs. TT = 1.00, 95 % CI 0.57-1.76, P OR = 0.994; ORCC vs. TT/TC = 0.88, 95 % CI 0.65-1.20, P OR = 0.425; ORCC/TC vs. TT = 0.98, 95 % CI 0.74-1.29, P OR = 0.861). Subgroup analyses by ethnicity further showed that there was no obvious association between CYP1A1 MspI polymorphism and endometrial cancer risk in both Caucasians and Asians. There was no obvious risk of publication bias. Therefore, the meta-analysis suggests that CYP1A1 MspI polymorphism is not associated with endometrial cancer risk.
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