Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

Objective To systematically evaluate the efficacy and safety of different administration methods of recombinant human endostatin(Endostatin)in the treatment of malignant pleural effusion in non-small cell lung cancer(NSCLC),and to provide more evidence-based bases for the clinical standardization of the use of Endostatin beyond the drug specification.Methods PubMed,The Cochrane Library,Web of Science,Embase,ChiCTR,VIP,CNKI,WanFang,and SinoMed databases were searched by computer for randomized controlled trials(RCT)of Endostatin alone or combined with chemotherapy for malignant pleural effusion in NSCLC.Network Meta-analysis was performed using Stata 14.0 software.Results A total of 50 RCTs involving 3 429 patients were included,covering 5 intervention measures.Network Meta-analysis showed that in terms of clinical effectiveness,there was no statistically significant difference between Endostatin(thoracic perfusion)+chemotherapeutic drug(thoracic perfusion or intravenous drip)and Endostatin(intravenous drip)+chemotherapeutic drug(thoracic perfusion or intravenous drip),and Endostatin(thoracic perfusion)and chemotherapeutic drug(thoracic perfusion)(P＞0.05);there were statistically differences between Endostatin(thoracic perfusion)+chemotherapeutic drug(thoracic perfusion or intravenous drip)and Endostatin(thoracic perfusion)[OR=3.44,95％CI(2.29,4.50),P＜0.05],and Endostatin(thoracic perfusion)+chemotherapeutic drug(thoracic perfusion or intravenous drip)and chemotherapeutic drug(thoracic perfusion)[OR=3.78,95％CI(3.16,4.51),P＜0.05](P＜0.05).The surface under the cumulative ranking curve(SUCRA)showed that Endostatin(thoracic perfusion)+chemotherapeutic drug(thoracic perfusion or intravenous drip)＞Endostatin(intravenous drip)+chemotherapeutic drug(thoracic perfusion or intravenous drip)＞Endostatin(thoracic perfusion)＞chemotherapeutic drug(thoracic perfusion)＞chemotherapeutic drug(intravenous drip).In terms of adverse effects,such as gastrointestinal reaction,and reduction of white blood cells and platelets,there was no statistically significant difference among the different interventions(P＞0.05).Conclusion Endostatin either by pleural instillation or combined with first-line chemotherapy drugs significantly improves clinical efficacy in malignant pleural effusion in NSCLC,and it is better and safer with thoracic perfusion efficacy.