Impacts of inhibiting Endostatin on the growth of SKOV_3 cell and it's mechanism / 中国癌症杂志

ABSTRACT

Background and purpose:Ovarian cancer is one of three common malignant tumors in the female reproductive system,whose mortality is the highest in all of the gynecological cancers.The genetic instability and hypermutation rate of tumor cells were found to be associated with chemotherapeutic resistance,and accounted for the high recurrence rate and the failure of current treatment.Invasion and metastasis of tumor are closely related to angiogenesis.Experiments in vivo and in vitro have confirmed that there are many kinds of promoter and suppressor of angiogenesis in primary malignant tumor cells.Angiogenesis could be a potential molecular target for cancer treatment.Endostatin is a specific inhibitor of vessel endothelium.Animal experiments have confirmed that Endostatin could inhibit tumor growth through anti-angiogenesis and result in the decrease of invasion and metastasis of cancer,and it would not easily induced drug resistance in the cells.Thus Endostatin could be safely used for a variety of cancer treatments,being able treat any patho-angiogensis.Recently it has been reported that Endostatin may significantly enhance anti-tumor effects when it is combined with traditional treatment methods such as surgery,chemotherapy,radiotherapy and immunotherapy.Although the study of Endostatin was done in vitro,the primary results were very encouraging and provide the rationale for future clinical trials.In this study,we aim to evaluate the inhibitory effect of Endostatin on SKOV_(3) cell and to investigate the possible mechanism of the inhibition.Methods:1.The effects of Endostatin on SKOV_(3) cells proliferation was studied by means!of MTT.2.The cell apoptosis and cell cycle were detected by transmission electron microscope and cell flow cytometry.3.bcl-2 and bax expression were determined in SKOV_(3) cell by immunocytochemistry,RT-PCR and Western blot analysis.Results:Endostatin inhibited SKOV_(3) cell proliferation,and the value of A_(490) of 15?g/ml 72 h Endostation group(0.454) was much lower than that of PBS control group(1.369)(P