Aim: To investigate the mechanism of anti-proliferation, anti-migration and anti-angiogenic effects of tanshinone ⅡA. Methods: In this study, MTT, 2-D/3-D migration, tube formation, PCR, chick embryo chorioallan-toic membrane (CAM) were used to evaluate the anti-proliferation, anti-migration and anti-angiogenic effects of tanshinone ⅡA. Results: Tanshinone ⅡA significantly inhibited the proliferation of human breast cancer line MDA-MB-435 with an IC_(50) of 21 nmol/mL And it is showed that breast cancer cells migration was effectively prevented by tanshinone ⅡA at 5 and 6 nmol/mL in a wound healing assay and a transwell migration assay. In ad-dition, tanshinone ⅡA inhibited the tube formation of newborn cattle aortic endothelial cells( NCAECs) after 2 h co-incubation with MDA-MB-435. These effects were not due to the inhibition of NCAECs proliferation; because tanshinone ⅡA non-selectively inhibited NCAECs growth with an IC_(50) of 124 nmol/mL Tanshinone ⅡA showed dose-dependent inhibitory effects on mRNA expression of VEGF and two transcription factors (HIF-1α/c-Myc) . Tashinone ⅡA was also found to inhibit angiogenic in vivo in the CAM assay. Conclusion: These results suggest that tanshinone ⅡA may exert its anti-proliferation, anti-migration and anti-angiogenic effects through down-regu-lating two transcription factors and VEGF. These novel anti-proliferations, anti-migrations, anti-angiogenic activi-ties of tanshinone ⅡA are likely to contribute to its cancer chemopreventive and therapeutic potential, especially in the treatment of breast cancer.

Objective To analyze the rule of lymph node metastasis, compare the preoperative computed tomographic findings with pathological diagnosis in thoracic esophageal carcinoma and to evaluate the clinical value. Methods Six hundred and eighteen patients with esophageal carcinoma after radical resection were enrolled. All patients did not receive any preoperative radiotherapy or chemotherapy, having complete information of postoperative pathological reports. CT scanning were applied to all patients in our hospital. The CT image were transmitted to the three-dimensional treatment planning system via the network at digital format and be reconstructed. In which system the sensitivity, specificity and accuracy rates in diagnosis of lymph node metastasis of the preoperative CT image were observed, measured and recorded. x2 test or Fisdher's statistical methods was adopted for comparing the concord rate of preoperative CT scanning with postoperative pathological diagnosis. Results Lymph nodes metastasis were defected in 242 of the 618 treated patients(39.2%), The rate of lymph node metastasis present in lower neck, upper-mediastinum,middle-mediastinum, lower-mediastinum, and superior abdomen regions in upper-thoracic esophageal carcinoma were 3.2% ,20.8% ,6.4% ,2.4% and 8.0%, in middle-thoracic esophageal carcinoma 1.5%,7.8% ,22.0% ,3.5% and 22.8%, and in lower-thoracic esophageal carcinoma 0% ,2.0% ,21.4% ,6.1% and 32.7%, respectively. The sensitivity, specificity, positive predictive value, negative predictive value,younden index and accuracy rates of diagnosis of lymph node metastasis with preoperative CT scan were 58.3%, 70.7%, 56.2%, 72.5%, 29.0% and 65.9%, respectively. The concordance rate of 0, 1, 2 and ≥ 3 lymph node metastasis by preoperative CT scanning with postoperative pathological diagnosis were 72.4%, 32.2% , 58.3% and 73.1%, respectively in whole group(x2 = 82. 61, P = 0.000). The concordance rate of no lymph node metastasis by CT scan comparing with that by postoperative pathological diagnosis was higher than that of the 1 lymph node metastasis in upper-thoracic esophageal carcinoma 3 lymph node metastasis were 71.1%, 30.1%, 55.6% and 77.8%, respectively(x2 =55.14,P =0.000.Conclusions Preoperative CT image can accurately predict the distribution patterns of the lymph node metastasis in esophageal carcinoma. The concordance rate was the highest in diagnosis of 0 and ≥3 lymph node metastasis, the lowest in diagnosis of one lymph node metastasis. These findings are valuable for definition of the target range of radiotherapy after radical resection of esophageal carcinoma.

ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L^-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L^-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L^-1 arrested the HCT116 cell cycle at G₀/G₁ phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 remarkably down-regulated the protein expression of CyclinD₁ （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L^-1 lowered the CyclinA₂ and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L^-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L^-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.

ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L^-1）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3β （GSK-3β）， c-Myc， survivin and Cyclin D₁. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D₁， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD₁ were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD₁ were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.