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The manifestation of a giant ovarian yolk sac tumor during late pregnancy is relatively rare. A yolk sac tumor is a highly malignant germ cell tumor that originates from primitive germ cells. It is characterized by yolk sac differentiation in vitro. The frequency of prenatal examinations should be appropriately increased for ovarian tumors discovered during pregnancy. Furthermore, regular follow-up ultrasound should be performed, and tumor markers should be dynamically detected. If needed, imaging examinations such as computed tomography and magnetic resonance imaging should be combined to comprehensively investigate disease progression. If the tumor diameter and tumor marker levels rapidly increase during pregnancy, the possibility of malignancy increases. Therefore, exploratory laparotomy should be immediately performed to further improve subsequent treatment modalities, early diagnosis, early treatment, and prognosis. Herein, we report the case of a 28-year-old pregnant woman whose pregnancy was terminated at 29 weeks and 5 days. She complained of lower abdominal pain for 2 days. A pelvic mass was detected for 1 week, accompanied by increased levels of tumor markers such as serum alpha-fetoprotein, cancer antigen 125, carbohydrate antigen 724, and human epididymis protein 4. Imaging revealed the presence of a pelvic mass. At 32 weeks and 3 days of pregnancy, a cesarean section was performed, with a transverse incision in the lower uterine segment. Furthermore, pelvic adhesiolysis, omentectomy, right adnexectomy, right pelvic lymph node dissection, and pelvic metastasis peritonectomy were performed. The postoperative pathological diagnosis was yolk sac tumors of the ovary (stage IIB). Postoperatively, a five-cycle chemotherapy regimen comprising bleomycin, etoposide, and cisplatin was administered. During postoperative follow-up, the patient’s general condition was noted to be good, with the newborn and pregnant women ultimately achieving good outcomes. We reviewed the relevant literature to increase clinical doctors’ understanding of ovarian malignancy during pregnancy, guide treatment selection, and facilitate early intervention for associated diseases.

In a prior study, our group found that chorionic villus-derived mesenchymal stem cells (CV-MSCs) were capable of promoting trophoblast proliferative and invasive activity. The mechanistic basis for this activity, however, has yet to be clarified. As such, an RNA-Seq analysis was conducted using trophoblasts that were treated with or without CV-MSC-conditioned media. Of the differentially expressed genes identified when comparing these two groups of cells, 23 proliferation-associated genes were identified and knocked down to test their functional roles in trophoblasts. These analyses revealed that inhibiting neuregulin 1 (NRG1) expression was sufficient to suppress proliferation and induce cell cycle arrest in trophoblasts. Placental samples from patients with preeclampsia exhibited significantly increased NRG1 expression relative to samples from healthy pregnancies. Following treatment with CV-MSC-conditioned media, NRG1 was upregulated in trophoblasts at the mRNA and protein levels. Relative to control trophoblasts, those in which NRG1 had been knocked down exhibited significantly impaired proliferation and DNA replication with the inactivation of the NF-κB signaling pathway. In contrast, overexpressing NRG1 yielded the opposite trophoblast phenotypes. Even in cells overexpressing NRG1, inhibition of NF-κB signaling was sufficient to significantly suppress trophoblast proliferation (P

Abstract Preeclampsia (PE), a pregnancy disorder that affects 5–7% of pregnant women, is among the primary causes for maternal and perinatal mortality. PE is believed to be associated with insufficient invasion of villous and extravillous trophoblasts (EVTs), which hampers uterine spiral artery remodeling and finally induces PE. But the mechanism responsible for reduction of trophoblast invasion remains unclear. In this study, placental tissues taken from healthy donors and PE patients were used to evaluate the miR-326 expression; CCK8 and colony formation assays were used to confirm the effect of miR-326 on cell proliferation; transwell assay was used to demonstrate the effect of miR-326 on cell invasion capability; western blot was used to investigate the underlying mechanism; and luciferase assay was used to detect the effect of miR-326 on YAP/TAZ-mediated transcription activity. It was revealed the miR-326 expression was higher in placentas from PE patients than from healthy donors. After transfection of miR-326 mimics, trophoblast proliferation and invasion were impaired. Using TargetScan, we speculated that PAX8 was a target of miR-326, which was later confirmed by western blot. The YAP/TAZ expression was also downregulated after transfection with miR-326. Luciferase assay demonstrated that overexpression of miR-326 suppressed YAP/TAZ-mediated transcription activity by targeting PAX8. Overexpression of PAX8 could partly rescue miR-326-induced suppression of trophoblast proliferation and invasion. Taken together, our result indicated that miR-326 suppresses trophoblast growth, invasion, and migration by means of targeting PAX8 via the Hippo pathway.