Objective To investigate the effect of dexamethasone combined with oridonin on proliferation and apoptosis in multiple myeloma cells U266 and the related molecular mechanism. Methods Exponential phase of growth U266 cells were treated with different concentrations of oridonin combined with dexamethasone or alone. U266 cells treated by DMSO were taken as control group. The proliferation inhibitory ratios were measured by CCK-8 assay followed by 24 h, 48 h and 72 h. Apoptosis induction was assessed by using Annexin V-FITC kit. Real time PCR was used to examine the mRNA changes of Notch1, NF-κB/p65 and bcl-2. Western blot assay was applied to detect the protein expression of Notch1, cleaved Notch1, NF-κB/p65 and bcl-2. Results Compared with that in control group, proliferation in all the experimental groups was inhibited (P<0.05), and the apoptosis was promoted (P<0.05); especially the combination of dexamethasone and oridonin had a synergistic effect on the proliferation and apoptosis of U266 cells (P<0.05). The results of PCR and Western blot showed that after treatment of U266 cells with dexamethasone, the mRNA as well as their protein levels of NF-κB/p65 and bcl-2 were decreased compared with those in the control group (P<0.05). Moreover, the mRNA and protein expression of Notch1, cleaved Notch1, NF-κB/p65 and bcl-2 was obviously down-regulated in oridonin group and the combination group (P<0.05). Conclusion Combination of dexamethasone and oridonin can significantly increase the anti-tumor effect by inhibiting proliferation and inducing apoptosis of U266 cells, which may be related to the inhibition of the Notch1 pathway.

Objective To explore the expression and significance of let-7a2 in lung adenocarcinoma.Methods To adapt technology of realtime PCR with reference of U6, the expression of let-7a2 in tumor tissues and normal tissues was detected in 15 cases of resected lung adenocarcinoma. The laboratorial data were analysed by measure of 2~(-△△CT) method. The analysed data were managed by statistics. Results The expression of let-7a2 in lung adenocarcinoma tissue was significantly lower than that in lung normal tissue (0.8733±0.4821 vs 2.4527±1.0111). This difference possess markedness significance(t=6.816, P<0.001).Conclusion The expression of let-7a2 in lung adenocarcinoma is obviously lower and is concerned with the course of lung cancer evolution.