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Oridonin, an ent-kaurene diterpenoid extracted from the traditional Chinese herb Rabdosia rubescens, has multiple biological and pharmaceutical functions and has been used clinically for many years. While the antitumor function of oridonin has been corroborated by numerous lines of evidence, its anticancer mechanism has not been well documented. In this study, the pancreatic cancer cell line BxPC-3 was used as a model to investigate a possible anticancer mechanism of oridonin through examining its effects on cell viability. The results showed that oridonin affected cell viability in a time- and dose-dependent manner. After exposure to different oridonin concentrations, growth rates and cell cycle arrest of BxPC-3 cells were significantly reduced compared with untreated cells, suggesting its effects on proliferation inhibition. Detailed signaling pathway analysis by western blot analysis revealed that low-dose oridonin treatment inhibited BxPC-3 cell proliferation by up-regulating p53 and down-regulating cyclin-dependent kinase 1 (CDK1), which led to cell cycle arrest in the G2/M phase. A high-dose oridonin not only arrested BxPC-3 cells in the G2/M phase but also induced cell accumulation in the S phase, presumably through γH2AX up-regulation and DNA damage. In addition, our results showed that a cell subpopulation was stained with propidium iodide after oridonin treatment. Protein quantification showed that cleaved poly(ADP-ribose) polymerase (PARP) expression was increased after a high-dose oridonin treatment, especially after long-term exposure. Accompanied by the increased level of deactivated PARP in BxPC-3 cells, the apoptosis initiators caspase-3 and caspase-7 expressions were also significantly increased, suggesting that caspase-mediated apoptosis contributed to cell death.

BackgroundOridonin, an ingredient used in traditional Chinese medicine, has been demonstrated to play an important role in antitumour effects, but the mechanism underlying its antitumour properties is still not clear.MethodsTo verify the anti-cancer effects of oridonin via a miRNA-dependent mechanism, comprehensive miRNA expression profiling of oridonin-treated BxPC-3 human pancreatic cancer cells was performed using a miRNA microarray assay based on Sanger miR-Base Release 20, followed by a validation using real-time PCR. MicroRNA target prediction and Gene Ontology and KEGG pathway analysis were performed to investigate possible pathways involved.ResultsThe results showed that 105 miRNAs were significantly differentially expressed (signal reading >500, p ≤ 0.01, |Log2-value| ≥1) in oridonin-treated BxPC-3 human pancreatic cancer cells.ConclusionsOur data indicates that oridonin inhibits BxPC-3 cells probably through regulating the expression of miRNAs. Interruption of miRNA profiling may provide new therapeutic methods for the clinical treatment of pancreatic cancer.

PD-L1 expression in pleural effusions (PE) of lung adenocarcinoma (ADC) was compared with pleural biopsies and the positive expression in PE was correlated with survival time. The matched slices from same patient’s pleura and PE were collected which both were pathologically verified positive. Immunohistochemistry (IHC) was used to detect PD-L1 expression. A total of 51 eligible cases were enrolled, including 30 males and 21 females. The average age was (67.06 ± 12.10) years. PD-L1 expression wasn’t statistically significant in pleura and cell masses (P > 0.05) and the correlation was statistically significant (r = 0.585, P = 0.000). Using an IHC scores of 5 point as a cutoff, positive PD-L1 expression in the pleura was 11.63% and that in the cell masses was 23.26%, and difference was significant (P < 0.05). The correlation coefficient was 0.605. Among 35 cases underwent systemic anti-tumor treatment, the mean survival time with positive PD-L1 expression in PE was 17.370 ± 1.827 months, which was significantly shorter than that with the negative (29.944 ± 2.671 months) (χ2 = 4.507, P = 0.034). Positive PD-L1 expression in PE is higher than in the pleura and their correlation is well. It may predict the short survival time after systemic anti-tumor treatment.