DEP domain containing 1 (DEPDC1) is a novel tumor-associated gene, which is aberrantly expressed in multiple types of cancer and involves in tumorigenesis and cancer progression. Here, we examined the functional involvement and underlying mechanism of DEPDC1 in breast cancer. In this study, the immunohistochemistry results demonstrated that DEPDC1 was high-expressed in breast cancer tissues compared with the paired adjacent normal breast tissues, and its tendency at protein level was consistent with mRNA level from TCGA data. Moreover, DEPDC1 mRNA level revealed the strongest association with poor prognosis and development in breast cancer. In vitro assays showed that DEPDC1 overexpression resulted in significant promotion of proliferation by regulating cell cycle in MCF-7 cells, whilst an opposite effect was found in the MDA-MB-231 cells with DEPDC1 deletion. Notably, further investigation indicated DEPDC1's ability of promoting breast cancer cells migration and invasion. In addition, we discovered that DEPDC1 caused hyper-activation of PI3K/AKT/mTOR signaling in breast cancer cells. Therefore, the increased DEPDC1 expression in breast cancer is correlated with disease progression and poor survival, which suggested that DEPDC1 might be a potential therapeutic target against this disease.

Gastric signet ring cell carcinoma (GSRCC) is a unique pathological type of gastric carcinoma that is extremely invasive and has a poor prognosis after diagnosis. The expression of microRNAs has been closely linked to the carcinogenesis of gastric cancer and has been considered as a powerful prognostic marker. Distinctive expression of miRNAs in GSRCC was investigated in the present study. Samples of GSRCC were compared to that of intestinal gastric adenocarcinoma using Agilent microarray technique, and two differentially expressed miRNAs were identified, hsa-miR-665 and hsa-miR‑95. qRT-PCR verification showed downregulation of both miRNAs in signet ring cell carcinoma and upregulation in gastric adenocarcinoma, which was not consistent with the results obtained by the microarray. Target gene prediction using online databases conferred two strong candidate genes, GLI2 and PLCG1. GO/KO analysis of these two genes showed close correlations with carcinogenesis and chemoresistance. It was concluded that hsa-miR-665 and hsa-miR-95 were downregulated in GSRCC but upregulated in intestinal gastric adenocarcinoma, and the relatively differential expression of the miRNAs negatively controlling their target genes could be closely related to the high invasive metastasis and chemoresistance of GSRCC.

Background and purposePremature ovarian insufficiency (POI) refers to a hypergonadotropic hypoestrogenism and the condition of pre-onset ovarian function failure. Epimedium is a common traditional Chinese herbal medicine that is widely used to relieve POI in China. To systematically explore the pharmacological mechanism of epimedium on POI therapy, a network pharmacology approach was conducted at the molecular level.MethodsIn this study, we adopt the network pharmacology method, which mainly includes active ingredients prescreening, target prediction, gene enrichment analysis and network analysis.ResultsThe network analysis revealed that 6 targets (ESR1, AR, ESR2, KDR, CYP19A1 and ESRRG) might be the therapeutic targets of epimedium on POI. In addition, gene-enrichment analysis suggested that epimedium appeared to play a role in POI by modulating 6 molecular functions, 5 cellular components, 15 biological processes and striking 52 potential targets involved in 13 signaling pathways.ConclusionThis study predicted the pharmacological and molecular mechanism of epimedium against POI from a holistic perspective, as well as provided a powerful tool for exploring pharmacological mechanisms and rational clinical application of traditional Chinese medicine.