PDP1 has been reported in multiple diseases. However, it has not been fully explored in ovarian cancer (OC). The public data was downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Differentially expressed gene analysis was conducted out using the limma package. Prognosis analysis was performed using the survival package. Gene Set Enrichment Analysis (GSEA) was performed using the fgsea package. Immune infiltration analysis was performed based on the CIBERSORT algorithm. CCK8 assay was used to evaluate the cell proliferation ability of cancer cells. Transwell assay was used for the invasion and migration ability. Our result showed that PDP1 was overexpressed in OC tissue in RNA and protein level based on multiple databases (TCGA, GSE18520, GSE27651, and GSE54388). At the same time, we found PDP1 was correlated with poor prognosis and worse clinical parameters. In vitro experiment showed that PDP1 could significantly promote proliferation, invasion, and migration ability of OC cells. GSEA analysis showed that in the OC patients with high PDP1 expression, the pathway of IL6/JAK/STAT3 signaling, interferon-alpha response, apoptosis, adipogenesis, KRAS signaling, and IL2/STAT5 signaling was activated, which might be responsible for its oncogenic effect in OC. Immune infiltration analysis indicated that PDP1 was positively correlated with activated myeloid dendritic cells, resting CD4 memory T cells, neutrophil, and M1 and M2 macrophages, yet negatively correlated with M0 macrophages, plasma B cells, γδT cells, and activated CD4 memory T cells. Drug sensitivity analysis showed a negative correlation between PDP1 expression and the IC50 of bleomycin and gemcitabine, yet a positive correlation of cisplatin, indicating that the OC patients with high PDP1 expression might be more sensitive to bleomycin and gemcitabine and more resistant to cisplatin. PDP1 could facilitate OC progression and is associated with patient prognosis and chemosensitivity, making it an underlying biomarker of OC.

Primary immune thrombocytopenia (ITP) is an autoimmune disease. However, the molecular mechanisms underlying ITP remained to be further investigated. In the present study, we analyzed a series of public datasets (including GSE43177 and GSE43178) and identified 468 upregulated mRNAs, 272 downregulated mRNAs, 134 upregulated lncRNAs, 23 downregulated lncRNAs, 29 upregulated miRNAs, and 39 downregulated miRNAs in ITP patients. Then, we constructed protein-protein interaction networks, miRNA-mRNA and lncRNA coexpression networks in ITP. Bioinformatics analysis showed these genes regulated multiple biological processes in ITP, such as mRNA nonsense-mediated decay, translation, cell-cell adhesion, proteasome-mediated ubiquitin, and mRNA splicing. We thought the present study could broaden our insights into the mechanism underlying the progression of ITP and provide a potential biomarker for the prognosis of ITP.