STROBE-GnRHa pretreatment in frozen-embryo transfer cycles improves clinical outcomes for patients with persistent thin endometrium: A case-control study.

The well-prepared endometrium with appropriate thickness plays a critical role in successful embryo implantation. The thin endometrium is the main factor of frozen-embryo transfer (FET), resulting in the failure of implantation undergoing FET. Hormone treatment is suggested to improve endometrium thickness; however, among the larger numbers of cases, it cannot reach the sufficient thickness, which leads to a high cancelation rate of embryo transfer as well as waste high-quality embryos. Thus, it increases the burden to patients in both economic and psychological perspectives. We performed a retrospective observational study, which was composed with 2 cohorts, either with the conventional hormone replacement therapy (HRT) protocol or HRT with gonadotrophin-releasing hormone agonist (GnRHa) pretreatment to prepare the endometrium before FET. The measurements of endometrium thickness, hormone level, transfer cycle cancelation rate, pregnancy rate, and implantation rate were retrieved from the medical records during the routine clinic visits until 1 month after embryo transfer. The comparisons between 2 cohorts were performed by t-test or Mann-Whitney U test depending on the different attributions of data. In total, 49 cycles were under HRT with GnRHa pretreatment and 84 cycles were under the conventional HRT protocol. HRT with GnRHa pretreatment group improved the endometrial thickness (8.13 ±â€…1.79 vs 7.51 ±â€…1.45, P = .031), decreased the transfer cancelation rate (P = .003), and increased clinical pregnancy rate and implantation rate significantly (both P = .001). Additionally, luteinizing hormone level in pretreatment group was consistently lower than conventional HRT group (P < .05). Our study revealed HRT with GnRHa pretreatment efficiently improved the endometrial thickness, therefore, decreased the FET cycle cancelation. It also elevated the embryo implantation rate and clinical pregnancy rate by improving endometrial receptivity.

The circular RNA PVT1/miR-203/HOXD3 pathway promotes the progression of human hepatocellular carcinoma.

Accumulating evidence suggests that circular RNAs (circRNAs) play important roles in various physiological and pathological processes. In the present study, we explored the role of circRNA PVT1 in hepatocellular carcinoma (HCC). qRT-PCR was performed to detect the relative expression of circPVT1 in HCC tissues and cell lines. The oncogenic roles of circPVT1 in HCC were evaluated by cell counting kit-8 (CCK-8) assay, ethynyl deoxyuridine (EdU) incorporation assays, transwell assays, flow cytometry and in vivo xenograft growth. Furthermore, bioinformatics, luciferase reporter assays and rescue experiments were conducted to determine the underlying mechanism of circPVT1 in HCC. Enhanced circPVT1 expression was detected in HCC tissues, which was closely associated with poor prognosis of patients with HCC. Knockdown of circPVT1 decreased the proliferation and migration ability of HCC cell lines in vitro Conversely, upregulation of circPVT1 improved the growth and migration in HCC cells. Mechanistically, we found that circPVT1 could bind directly to miR-203 and contributed to the initiation and progression of HCC by regulating miR-203/homebox D3 (HOXD3) pathway. In conclusion, our study reveals that circPVT1 participates in the progression of HCC through the miR-203/homeobox D3 (HOXD3) pathway and might represent a potential therapeutic target for HCC treatment.

Genome-wide screening identifies oncofetal lncRNA Ptn-dt promoting the proliferation of hepatocellular carcinoma cells by regulating the Ptn receptor.

Oncofetal genes are genes that express abundantly in both fetal and tumor tissues yet downregulated or undetected in adult tissues, and can be used as tumor markers for cancer diagnosis and treatment. Meanwhile, long noncoding RNAs (lncRNAs) are known to play crucial roles in the pathogenesis of hepatocellular carcinoma (HCC), including tumor growth, proliferation, metastasis, invasion, and recurrence. We performed a genome-wide screening using microarrays to detect the lncRNA expression profiles in fetal livers, adult livers, and liver cancer tissues from mice to identify oncofetal lncRNAs in HCC. From the microarray data analysis, we identified lncRNA Ptn-dt as a possible oncofetal gene. Both in vitro and in vivo experiments results confirmed that overexpression of Ptn-dt significantly promoted the proliferation of mouse HCC cells. RNA pulldown assay showed that Ptn-dt could interact with the HuR protein. Interestingly, miR-96 binds with HuR to maintain its stability as well. Overexpression of lncRNA Ptn-dt led to the downregulation of miR-96, which might be due to the interaction between Ptn-dt and HuR. Meanwhile, previous studies have reported that Ptn can promote tumor growth and vascular abnormalization via anaplastic lymphoma kinase (Alk) signaling. In our study, we found that overexpression of Ptn-dt could promote the expression of Alk through repressing miR-96 via interacting with HuR, thus enhancing the biologic function of Ptn. In summary, a new oncofetal lncRNA Ptn-dt is identified, and it can promote the proliferation of HCC cells by regulating the HuR/miR-96/Alk pathway and Ptn-Alk axis.

[Polypronuclear zygotes and clinical pregnancy after IVF].

OBJECTIVE: To study the relationship between the percentage of polypronuclear zygotes and clinical pregnancy following IVF. METHODS: We collected the data of 954 IVF cycles, and according the percentage of polypronuclear zygotes in the IVF cycles, allocated them to Groups A (without polypronuclear zygotes) , B (with < 30% polypronuclear zygotes) and C (with > or = 30% polypronuclear zygotes). Then we analyzed the relationship between the percentage of polypronuclear zygotes and the rate of clinical pregnancy. RESULTS: Compared with Group A, Group C showed a significantly lower rate of clinical pregnancy (43.2% vs 28. 1%, P < 0.05), while Group B exhibited a markedly higher rate (43.2% vs 52.36%, P < 0.05) and obviously decreased polypronuclear zygote formation with the increase of age (35.6% vs 24.1%, P < 0.05). CONCLUSION: The percentage of polypronuclear zygotes in IVF cycles may serve as a prognostic indicator of the clinical outcome.