Title of article :
Suppression of gelatinase production with decreased invasiveness of choriocarcinoma cells by human recombinant interferon beta
Author/Authors :
Noriko Kato، نويسنده , , Akihiro Nawa، نويسنده , , Koji Tamakoshi، نويسنده , , Fumitaka Kikkawa، نويسنده , , Nobuhiko Suganuma، نويسنده , , Tomomitsu Okamoto، نويسنده , , Setsuko Goto، نويسنده , , Yutaka Tomoda، نويسنده , , Michinari Hamaguchi، نويسنده , , Motowo Nakajima، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1995
Pages :
6
From page :
601
To page :
606
Abstract :
OBJECTIVE: Choriocarcinoma is a highly invasive gynecologic tumor, and hematogenous metastases frequently develop. To establish a molecular basis for antiinvasion therapy of choriocarcinoma, we examined the effects of human recombinant interferons on gelatinase production and invasion by choriocarcinoma cells. STUDY DESIGN: Using the five choriocarcinoma cell lines, we measured gelatinase activity by gelatin zymography. The effects of recombinant interferons (rIFN-α, riFN-β, and rIFN-γ) were then analyzed by Western blot analysis and chemoinvasion assay. RESULTS: High levels of 72 kd gelatinase activity were detected in the highly invasive choriocarcinoma cell lines, two of which also contained an active form of 72 kd gelatinase with an apoparent molecular mass of 88 kd. Gelatinase production was decreased by incubation with rIFN-β. In the chemoinvasion assay, only rIFN-β had an inhibitory effect on the invasiveness of tumor cells without a cytotoxic effect. CONCLUSION: Choriocarcinoma cells showed high 72 kd gelatinase activity, which suggested a role for the enzyme in vascular metastasis. Studies on the use of rIFN-β to inhibit metastasis of choriocarcinoma via suppressio of gelatinase production are warranted.
Keywords :
72 kd gelatinase , Choriocardnoma , human recombinant interferon-t3 , invasiveness
Journal title :
American Journal of Obstetrics and Gynecology
Serial Year :
1995
Journal title :
American Journal of Obstetrics and Gynecology
Record number :
638583
Link To Document :
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