ObjectiveAberrant expression of the immune checkpoint molecule, CD276, also known as B7-H3, is associated with tumorigenesis. In this review, we aim to comprehensively describe the role of CD276 in malignancies and its potential therapeutic effect.Data SourcesDatabase including PubMed, EMbase, Cochrane Library, CNKI, and Clinical Trails.gov were searched for eligible studies and reviews. Study selection: Original studies and review articles on the topic of CD276 in tumors were retrieved.ResultsCD276 is an immune checkpoint molecule in the epithelial mesenchymal transition (EMT) pathway. In this review, we evaluated the available evidence on the expression and regulation of CD276. We also assessed the role of CD276 within the immune micro-environment, effect on tumor progression, and the potential therapeutic effect of CD276 targeted therapy for malignancies.ConclusionCD276 plays an essential role in cell proliferation, invasion, and migration in malignancies. Results from most recent studies indicate CD276 could be a promising therapeutic target for malignant tumors.

BackgroundFew patients with prostate cancer benefit from current immunotherapies. Therefore, we aimed to explore new strategies to change this paradigm.MethodsHuman tissues, cell lines and in vivo experiments were used to determine whether and how N-cadherin impacts the production of programmed death ligand-1 (PD-L1) and indole amine 2,3-dioxygenase (IDO-1) and whether N-cadherin can increase the production of effector (e)Treg cells. Then, we used PC3-bearing humanized non-obese diabetic/severe combined immunodeficiency IL2Rγnull (hNSG) mice with an intravenous injection of human CD34+ hematopoietic stem cells into the tail vein to evaluate whether the N-cadherin antagonist N-Ac-CHAVC-NH2 (designated ADH-1) could improve the therapeutic effect of tumor-infiltrating lymphocyte (TIL)-related treatment.ResultsN-cadherin dramatically upregulated the expression of PD-L1 and IDO-1 through IFN-γ (interferongamma) signaling and increasing the production of free fatty acids that could promote the generation of eTreg cells. In preclinical experiments, immune reconstitution mediated by TILs slowed tumor growth and extended the survival time; however, this effect disappeared after immune system suppression by PD-L1, IDO-1 and eTreg cells. Furthermore, ADH-1 effectively reduced immunosuppression and enhanced TIL-related therapy.ConclusionsThese data show that the N-cadherin antagonist ADH-1 promotes TIL antitumor responses. This important hurdle must be overcome for tumors to respond to immunotherapy.

Background: The underutilization of additional supportive muscles is one of the potential reasons for suboptimal efficacy of conventional pelvic floor muscle training (CPFMT). The present study concentrates on any advantage of advanced pelvic floor muscle training (APFMT) in patients with urinary incontinence (UI) after radical prostatectomy (RP). Methods: Literature search was conducted on PubMed, Embase, Cochrane Library and Web of Science from database inception to February 2020. The data analysis was performed by the Cochrane Collaboration's software RevMan 5.3. Results: Both APFMT and CPFMT groups indicates superiority over baseline in terms of pad number, the International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF) score, pad weight at short-term follow-up, and PFME and PFMS at intermediate-term follow-up. No adverse events were reported in all included studies. Patients receiving APFMT had a similar attrition rate to those receiving CPFMT (18/236 vs. 22/282, P=0.61). Compared to CPFMT group, APFMT group provided intermediateterm advantages in terms of pad number (MD: −0.75, 95% CI: −1.36 to −0.14; P=0.02), ICIQ-SF score (MD: