Trophoblasts are important parts of the placenta and exert vital roles in the maternal‐foetal crosstalk, and sufficient trophoblasts migration and invasion is critical for embryo implantation and normal pregnancy. Macrophages, as the major components of decidual microenvironment at maternal‐foetal interface, can interact with trophoblasts to participate in the regulation of normal pregnancy. Previously, our group have demonstrated that trophoblasts could induce macrophages polarization to M2 subtype by secreting interleukin‐6 (IL‐6); however, the understanding of macrophages regulating the migration and invasion of trophoblasts is limited. In the present study, we used the co‐cultured model to further investigate the effects of macrophages on trophoblasts migration and invasion. Our results showed that co‐culture with macrophages promoted epithelial‐to‐mesenchymal transition (EMT) of trophoblasts, thereby enhancing their migrative and invasive abilities. Further experiments revealed that M2 macrophage‐derived G‐CSF was a key factor, which promoted the EMT, migration and invasion of trophoblasts via activating PI3K/Akt/Erk1/2 signalling pathway. Clinically, G‐CSF was highly expressed in placental villous tissues of normal pregnancy patients compared to patients with recurrent spontaneous abortion, and its expression level was significantly correlation with EMT markers. Taken together, these findings indicate the important role of M2 macrophages in regulating trophoblasts EMT, migration and invasion, contributing to a new insight in concerning the crosstalk between macrophages and trophoblasts in the establishment and maintenance of normal pregnancy.

Background: Polycystic ovarian syndrome (PCOS) is an endocrine-related disease related to abnormal folliculogenesis and is a leading cause of infertility worldwide. Inhibition of granulosa cells (GCs) proliferation and increased GCs apoptosis have been identified as the major factors in aberrant follicle maturation.Methods: USP25 and PTEN expression in GCs from women with and without PCOS was analyzed using Western blotting. A PCOS-like mouse model was constructed using USP25 knockout and wild-type mice to explore the role of USP25 in PCOS. The human granular cell line KGN was cultured for proliferation and apoptosis assays, and the effect of USP25 on PTEN was investigated after transfection with shRNA-USP25 lentivirus.Results: USP25 expression was found to be elevated in patients and mice with PCOS. With mouse model, we observed a reduction in PCOS symptoms in mice after USP25 deletion. Increased proliferation, reduced apoptosis, activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and decreased PTEN expression were found in KGN cells after USP25 knockdown. Finally, we verified that USP25 could deubiquitinate PTEN in KGN cells.Conclusions: In this study, we investigated that USP25 can regulate the PI3K/AKT signaling pathway by deubiquitinating PTEN, thus affecting the proliferation and apoptosis of GCs and contributing to the pathogenesis of PCOS.

MicroRNAs (miRNAs), as a class of small, well-conserved, non-coding RNA molecules, hold the capacity to post-transcriptionally suppress the expression of over 50% protein-coding genes. Emerging and accumulating evidence suggests that miRNAs function as the master regulators of multiple pathophysiological processes, and play important roles in diverse human diseases, especially in tumorigenesis and progression. MiR-106b-5p, a member of miR-106b seed family, has been demonstrated to be aberrantly expressed in human solid malignancies, and to play paradoxically opposing functions as an oncomiR or a tumor suppressor in tumor development. In addition, it has been recently reported to be a promising biomarker for prognostic evaluation for cancer patients. In the present review, we provided an overview to summarize the present findings of miR-106b-5p in cancer research fields, thereby establishing comprehensive understanding of its diverse functions and clinical implications in human cancers.

Background: Endometriosis is a major contributor to infertility and pelvic pain, which brings a significant burden on family and society. Although the data of endometriosis in Global Burden of Disease (GBD) 2019 was reviewed, no updated analysis has been conducted using GBD 2021, and the disease burden across different age groups has not been analyzed. The aim of this cross-sectional analysis was to provide an up-to-date assessment of the prevalence, incidence, and disability-adjusted life-years (DALYs) of endometriosis from 1990 to 2021 at the global, national, and regional levels. Material and methods: We obtained data on the prevalence, incidence, and DALYs of endometriosis from GBD 2021. These data were analyzed to provide an overview of the epidemiological trends and disease burden of endometriosis in 204 countries and regions worldwide from 1990 to 2021, and we projected trends through 2040. Health inequality analysis, joinpoint regression analysis, and decomposition analysis were applied to data assessment. Results: In 2021, the global burden of endometriosis remained substantial, with a total of 22.28 million cases (95% UI: 13.67, 33.69), corresponding to an age-standardized prevalence rate (ASPR) of 1023.8 per 100 000 (95% UI: 627.36, 1549.77). The age-standardized incidence rates (ASIR) was 162.71 (95% UI: 85.21, 265.35) per 100 000, while the age-standardized DALY rate (ASDR) was 94.25 (95% UI: 50.82, 157.73) per 100 000. Regionally, areas with low sociodemographic index (SDI) experienced the highest ASPR, ASIR, and ASDR, while high SDI regions exhibited the lowest rates. Geospatially, Oceania and Eastern Europe displayed the highest ASPR, ASIR, and ASDR. Among countries, Niger had both the highest ASPR and ASDR, and Solomon Islands had the highest ASIR. Women aged 25–29 years emerged as the most affected group, suggesting that this cohort should be a key focus for interventions. By 2040, the global ASPR of endometriosis is projected decline to 887.89 per 100 000 (95% CI: 530.79, 1245), representing a decrease of 13.28% from 2021. Decomposition analysis showed population growth was the major contributing factor, followed by epidemiologic change. Conclusion: While the burden of endometriosis has decreased globally from 1990 to 2021, significant disparities remain, especially in low SDI regions. It is necessary to develop better policies and preventive measures to effectively address the range of problems associated with endometriosis.