Background Bone morphogenetic protein receptor II (BMPR-II) plays an important role in tumor’s invasion and proliferation. In this study, we observed the effects of small interfering RNA (siRNA) targeting bone morphogenetic protein receptor II (BMPR-II) on the biological activities of human liver cells and explore its mechanism. Methods The molecular sequences of three siRNA targeting BMPR-IIwere designed and synthesized. In this study, there were 6 groups including group I (normal control), group II (blank control), group III (negative control) and group IV-VI (BMPR-II-siRNA-a, siRNA-b and siRNA-c-transfected cells, respectively). The levels of mRNA and protein of BMPR-II were determined to select the best sequence for BMPR-II silence. After liver cancer cells were transfected with the best sequence, proliferation and invasion of transfected cells were assessed, and apoptosis and cell cycle were detected. The expressions of mitogen-activated protein kinases (MAPKs) signal pathway-related VEGF-C protein were observed after BMPR-II silence and BMPR-II silence combined with inhibiting MAPKs signal pathway, respectively. Results RT-PCR and Western blot indicated that BMPR-II expression was the highest in HepG2 among the three liver cancer lines ( P < 0.01) and the lowest in group IV among the six groups ( P < 0.01). MTT assay and transwell assay revealed that the numbers of cell growth and cell transmembrane were significantly lower in group IV than in control groups 48 h after cells were transfected ( P < 0.05). Flow cytometer showed that apoptosis was the highest and cells were significantly blocked in S phase 48 h after cells were transfected in group IV ( P < 0.01). Western blot indicated that the protein levels of p-P38 ( P < 0.01) and vascular endothelial growth factor-C (VEGF-C) ( P < 0.01) were significantly decreased after BMPR-II silence. The protein level of VEGF-C was significantly decreased in PD98059 + siRNA-BMPR-II-a and SB203580 + siRNA-BMPR-II-a groups ( P < 0.01), especially in SB203580 + siRNA-BMPR-II-a group ( P < 0.01). Conclusions siRNA targeting BMPR-IIcan markedly inhibit HepG2 proliferation and invasion, promote apoptosis and block HepG2 in S phase. Its mechanism may be that BMPR-II silence down-regulates VEGF-C expression through MAPK/P38 and MAPK/ERK1/2 pathways, especially MAPK/P38. This study provides a new targeted therapy for liver cancer.

Objective To investigate the physical and functional relation between ERɑ and p73ɑ in breast cancer cells.Methods Protein expressions of ERɑ and p73ɑ were examined by Western Blot.The binding assay for ERɑ and p73ɑ was tested with Co-IP and immunoblot.Transcriptional activity of ERɑ and p73ɑ was analysed by Luciferase assay.Results and Conclusion(1)ERɑ and p73ɑ can bind to each other.(2)ERɑ and p73ɑ can be combined to form complex and mutually inhibit protein expression of each other in breast cancer cells.

p53基因是目前研究最多的肿瘤抑制基因之一,它与肿瘤的发生、发展关系密切,基于p53基因的抗肿瘤治疗已逐渐成为抗肿瘤治疗的重要方法之一。活化的p53可引起细胞周期静止,细胞凋亡或者细胞老化,而细胞老化和抗肿瘤之间存在着密切的关系,本文将对p53诱导细胞老化的最新进展作一综述。