Ovarian cancer is highly malignant with a gradually increasing incidence and a high mortality rate. Immunosuppression is induced in ovarian cancer, although the mechanism detail is not clear. It has been indicated that HVEM (herpesvirus entry mediator) B- and T-lymphocyte attenuator (BTLA) negatively regulates the immune responses of T lymphocytes. Here, HVEM mRNA was found to be elevated in ovarian cancer tissue samples and primary ovarian cancer cells in comparison with benign tissue samples. We then knocked down HVEM expression in an ovarian cancer cell line, OVCAR3, by lentivirus-based small hairpin RNA (shRNA). Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis showed that HVEM-shRNA had no effect on the proliferation, early apoptosis, or cell cycle distribution of OVCAR3. We then isolated activated T cells and performed coculture experiments in Transwell. Remarkably, HVEM-silenced ovarian cancer cells (primary ovarian cancer cells and OVCAR3) increased the number of T cells and the secretion of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), while activated T cells promoted the apoptosis of HVEM-silenced ovarian cancer cells. The current study partially explains the immune escape mechanism of ovarian cancer cells and provides a possible target for immunotherapy.

Epithelial ovarian cancer (EOC) prognosis is associated with International Federation of Gynecology and Obstetrics (FIGO) staging, cancer cell classification, patient age, and residual tumor size. However, the molecular markers for predicting EOC prognosis remain to be explored. In this study, we investigated the expression of CD24, COX-2, and p53 in EOC, and their relationships to clinical prognosis. We found that the expression of CD24 was detected in the cell membrane in 90.6 percent (58/64) of EOC cases and in the cytoplasm in 54.7 percent (35/64) of EOC cases; 78.6 percent (11/14) cases of borderline tumors had CD24-positive staining in the cell membrane. All 9 cases of benign tumors were negative for CD24 staining. Expression of CD24 correlated with the nuclear expression of p53, but not with the expression of COX-2. Overexpression of CD24 is an independent factor associated with tumor metastasis, a low survival rate, and a short survival time. Our results suggest that CD24 may be a valuable molecular marker for predicting prognoses of patients with EOC.

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Acute respiratory distress syndrome (ARDS) is very common in patients with severe acute pancreatitis (SAP), the early interventions are essential to the prognosis of SAP patients. We aimed to evaluate the risk factors for ARDS in SAP patients, to provide insights into the management of SAP. SAP patients treated in our hospital from June 1, 2018 to May 31, 2020 were included. The characteristics and lab test results were collected and compared, and we conducted the logistic regression analyses were conducted to identify the potential risk factors for ARDS in patients with SAP. A total of 281 SAP patients were included finally, the incidence of ARDS in patients with SAP was 30.60%. There were significant differences on the respiratory rate, heart rate, APACHE II and Ranson score between 2 groups (all P < .05). And there were significant differences on the polymorphonuclear, procalcitonin, C-reactive protein, serum creatinine, albumin and PO2/FiO2 between 2 groups (all P < .05), and no significant differences on the K+, Na+, Ca+, white blood cell, neutrophils, urine and blood amylase, trypsin, lipase, alanine aminotransferase, aspartate aminotransferase, total bilirubin, triglyceride, total cholesterol, total bilirubin, fasting blood glucose, and pH were found (all P > .05). Respiratory rate >30/min (odds ratio [OR]: 2.405, 95% confidence interval[CI]: 1.163–4.642), APACHE II score >11 (OR: 1.639, 95% CI: 1.078–2.454), Ranson score >5 (OR: 1.473, 95% CI: 1.145–2.359), polymorphonuclear >14 × 109/L (OR: 1.316, 95% CI: 1.073–2.328), C-reactive protein >150 mg/L (OR: 1.127, 95% CI: 1.002–1.534), albumin ≤30 g/L (OR: 1.113, 95% CI: 1.005–1.489) were the independent risk factors for ARDS in patients with SAP (all P < .05). The incidence of ARDS in SAP patients is relatively high, and it is necessary to carry out targeted early prevention and treatment for the above risk factors.

Background: Our previous studies showed the expression of herpes virus entry mediator (HVEM) is high in ovarian cancer samples and correlated to the patient clinic pathological features. As we all know, the hypoxic environment is the main feature of tumor. In this work, we explored the role of HVEM in hypoxic ovarian cancer cells and its effects on HIF-1α, a transcription factor responding to hypoxia. Methods: The expression of HVEM, HIF-1α and apoptosis-related genes was detected by qRT-PCR and western blot. The proliferation and apoptosis of the ovarian cancer cells were determined with the Cell Counting Kit-8 assay and AnnexinV-FITC/PI-stained flow cytometry assay, respectively. Results: The expression of HVEM was positively correlated to that of HIF-1α. The expression of HVEM and HIF-1α under hypoxic conditions was higher than that under normoxic conditions, which suggested that the level of HVEM and HIF-1α correlates with prolonged periods of hypoxia in ovarian cancer. The overexpression of HVEM promoted cell proliferation and inhibited cell apoptosis under hypoxic condition. HVEM overexpression elevated the expression of HIF-1α and Bcl-2 (anti-apoptotic protein), and reduced the expression of Bax (pro-apoptotic protein). In addition, overexpression of HVEM activated the AKT/mTOR signaling. Moreover, knockdown of HVEM had the completely opposite effects. Conclusion: These data indicated that HVEM signaling might promote HIF-1α activity via AKT/mTOR signaling pathway and thus to regulate tumor growth in ovarian cancer under the hypoxic conditions. Furthermore, these findings indicate that this molecular mechanism could represent a therapeutic target for ovarian cancer.