ObjectiveTo investigate the effects of Saposhnikovia divaricata extract combined with arsenic trioxide (ATO) on the proliferation and apoptosis in chronic myelogenous leukemia K562 cells. MethodsSaposhnikovia divaricata extract was prepared.Cultured K562 cells were treated with different concentration of Saposhnikovia divaricataextract or/and ATO for 48h. Cell proliferation was determined using the MTT assay. Apoptosis and cell cycle were detected using flow cytometry.ResultsThe MTT assay showed that Saposhnikovia divaricata extract of 750,1 000,1 250,1 500 μg/ml had a significantly proliferation inhibitory effect compared with control group, the inhibitory rates were 23.29% ± 3.31%, 48.30% ± 2.50%, 79.62% ± 3.41% and 88.94% ± 0.06%, respectively (allP<0.05); Saposhnikovia divaricata extract of 500 μg/ml combined with ATO of 1.0, 0.5 μg/ml significantly increased inhibitor rates compared with ATO of 1.0, 0.5 μg/ml (64.99% ± 5.18%vs. 44.48% ± 3.31%,38.59% ± 3.88%vs.26.30% ± 5.03%; allP<0.05). FCM showed that Saposhnikovia divaricata extract of 500 μg/ml combined with ATO of 2.0, 1.0, 0.5 μg/ml significantly increased apoptotic rate compared with ATO group of 2.0, 1.0, 0.5 μg/ml (33.97% ± 0.59%vs.20.97% ± 2.17%, 13.53% ± 0.47%vs.9.77%±0.64%、6.63%±&0.40%vs.4.00%±0.46%; allP<0.05 ). Cell cycle results showed that Saposhnikovia divaricata extract of 500μg/ml combined with ATO of 2.0,1.0, 0.5μg/ml significantly increased the rate of S phase compared with ATO group of 2.0, 1.0, 0.5 μg/ml (60.25 ± 2.59%vs.55.61 ± 1.28%, 60.89 ± 1.53%vs.37.96 ± 1.02%, 47.76 ± 0.87%vs.39.90 ± 0.92%; allP<0.05).ConclusionsSaposhnikovia divaricataextract could obviously inhibit the proliferation of K562 cells and enhance the apoptotic effect of ATO. ATO could induce a G2/M phase arrest, while Saposhnikovia divaricata extract combined with ATO could induce a S phase arrest in K562 cells.

Objective To study the effect of black granule capsules(BGCs) on growth of transplanted mouse hepatocarcinoma cells, cell proliferation cycle and apoptosis.Methods KM mouse were subcutaneously inoculated with Hepatocarcinoma cells (H22) and randomly divided into the model control group, the positive control group, the low, medium and high does of BGC group after 24h. The positive control group received intraperitoneal injection with 30 mg/kg cyclophosphamide. Mice of BGC groups were intragastricaly with different dosage of BGC (400, 800, 1 600 mg/kg). The model control group received intragastricaly with normal saline. The drugs were administrated once a day for seven days. The tumor inhibition rate was calculated at 24 h after the last administration. Flow cytometry was used to detect changes of cell cycle and apoptosis in harvested H22 tumor cells.Results The group of high does showed significant inhibitory effect on the growth of transplanted H22 tumor cells withthe inhibitory rate 38.78% (male) and 43.57% (female). Compared with model control group, groups of different dosages decreased time of G0-G1 phase (58.06% ± 9.65%, 55.10% ± 5.89%, 61.36% ± 15.95%vs. 74.47% ± 2.63%), increased tiem of Sphase (33.96% ± 11.90%, 32.67% ± 4.04%, 33.89% ± 9.82%vs. 14.37% ± 4.92%), and increased the apoptosis rate (31.12% ± 1.85%, 31.89% ± 2.16%, 40.64% ± 0.55%vs.21.75% ± 2.64%).Conclusion BGC has antitumor effect on mouse hepatocarcinoma H22 tumor cells, and its mechanism was to regulate cell proliferation cycle and induce the apoptosis.

OBJECTIVE: To observe wether pSIREN-survivin/shRNA can induce the apoptosis and inhibit it's growth of nude mice xenograft tumor of nasopharyngeal carcinoma cell. METHOD: Subcutaneous tumors in athymic mice were induced by inoculation of NPC and divided into the blank group A, the negative group B,the experimental group C randomly. PBS,the negative and positive pSIREN-survivin/shRNA were injected into the subcutaneous tumors poly site. The inhibition ratio was measured by the tumor size calculation after inoculation. The expression of survivin in the xenograft tumor was observed by RT-PCR and immunohistochemistry. The cell apoptosis in tumor tissues was detected by TEM. The liver and kidney function was tested by blood routine test. RESULT: The inhibition ratio of group C and group B was (52. 11 +/- 1. 03)%, (2. 15 0. 11)% respectively, the inhibition rate in expression level of survivin mRNA was (77. 5+/-2. 03) %, (1. 39+/-0. 14) % respectively. The dyeing of survivin was more shallow in group C, the intensity is also less than group B. Nuclear chromatin was deepened, split into pieces, flake, and nuclear membrane was surrounded to edge. Cytoplasmic color and density were deepened, and organelles such as mitochondria was disappeared, the microscopic changes of cellular apoptosis at the earlier stage were watched, the difference of the function in liver and kidney was not statistically in statistical. CONCLUSION The expression of survivin in xenograft tumor was significantly inhibited by pshRNA-survivin/shRNA,the apoptosis of tumor cells was accelerated and the growth speed of NPC cells in xenograft tumor was retarded. The high expression of nasopharyngeal carcinoma's gene could significantly be silenced by using technology of RNAi, the growth of tumors could be inhibited also. Its a novel treatment that have a good prospect.
Animals ; Apoptosis ; Carcinoma ; Cell Line, Tumor ; Cell Proliferation ; Female ; Gene Silencing ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; Mice ; Mice, Nude ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; pathology ; RNA, Small Interfering ; genetics ; Survivin ; Xenograft Model Antitumor Assays

OBJECTIVE: To evaluate the treatment and prognosis of sinonasal mucosal melanoma (SMM). METHOD: Clinicopathological data of SMM patients from January 1976 to December 2005 were analyzed retrospectively. Survival analysis was performed and Kaplan-Meier analysis was used to compare the effect of clinicopathological factors on survival using SPSS 18.0 software. A Cox model was applied for multivariate analysis. RESULT: The 3-year and 5-year overall survival (OS) rates of 68 cases of SMM were 36.1% and 29.4%, respectively. The 3-year and 5-year OS of patients who underwent surgery or biotherapy were significantly higher than that of patients who underwent other therapeutic regimens without surgery or without biotherapy, respectively. Multivariate analysis showed the patients with distant metastasis at first present or residual/recurrence had a worse prognosis than that without distant metastasis or residual/recurrence, respectively. Surgery and biotherapy were effective treatments for SMM. CONCLUSION SMM has a poor prognosis, especially in the patients with distant metastasis or residual/recurrence. Surgery or biotherapy may improve the prognosis of patients with SMM.
Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; Female ; Humans ; Male ; Melanoma ; diagnosis ; therapy ; Middle Aged ; Nasal Mucosa ; Nose Neoplasms ; diagnosis ; therapy ; Prognosis ; Retrospective Studies ; Treatment Outcome ; Young Adult