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Effects and mechanisms of endostatin on the growth of ovarian cancer SKOV3 cells in vitro and in vivo

  • Published:
Chinese Journal of Cancer Research

Abstract

Objective

To evaluate the inhibitory effect of Endostatin on ovarian cancer cell line SKOV3 and to investigate the possible mechanism of the inhibition.

Methods

Using MTT, transmission electron microscope (TEM) and immunocytochemistry, the effects of Endostatin on the proliferation of SKOV3 cells were studied. Nude mice were subcutaneously implanted with SKOV3 cells. The cell apoptosis of implanted tumor was detected by TUNEL and TEM. The expressions of bcl-2 and bax in implanted tumor tissues were measured by RT-PCR and immunohistochemistry.

Results

Endostatin significantly inhibited the proliferation of SKOV3 cells in vitro (P<0.01) and induced cell apoptosis, whereas the expressions of bcl-2 and bax were not changed obviously in SKOV3 cell treated with Endostatin. The mean tumor weight of Endostatin treated group was markedly lower than that of PBS control group (P<0.05). The expression of bcl-2 was down-regulated in Endostatin treated group, but bax was not influenced.

Conclusions

The results demonstrated that Endostatin might have anti-tumor effect on ovarian carcinoma. One of the important mechanisms of Endostatin effect of anti-angiogenic and anti-tumor activities might involve regulating the bcl-2/bax expression and inducing apoptosis.

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Authors

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Correspondence to Sui Li-hua  (隋丽华).

Additional information

Foundation item: This work was supported by the Key Problem Research Project of Hei-Long-Jiang Province(No. 20020101).

Biography: LIU Mei-mei(1977–), female, candidate doctor of medicine, The Second Affiliated Hospital, Harbin Medical University, majors in gynecology.

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Mei-mei, L., Li-hua, S., Pei-ling, L. et al. Effects and mechanisms of endostatin on the growth of ovarian cancer SKOV3 cells in vitro and in vivo . Chin. J. Cancer Res. 18, 132–137 (2006). https://doi.org/10.1007/s11670-006-0132-8

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  • DOI: https://doi.org/10.1007/s11670-006-0132-8

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