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A new perspective for the treatment of human endometrial cancer
POLLIO ML1, RUGGIERO MG1, IACOBELLIS F3, MANCINI R2, FORESTI M1, BORRELLI A2,
SCHIATTARELLA A1, COLACURCI N4, COBELLIS L4, MANCINI A2, PICA A.1
1Department of Biology, University of Naples Federico II.
2NCI,Pascale Foundation,Naples.
3Department of Exp and Clin Medicine Magrassi-Lanzara, SUN, Naples
4Department of Gynecology, SUN, Naples.
The endometrial cancer is one of the principal causes of death in women (Siegel et al., 2012). The
main treatment for this cancer is hysterectomy that involves loss of fertility (Holland, 2008). If the
tumor is not well defined and metastasizes, radio/chemo therapy are needed. The survival after
chemotherapy is about 5-10 years, because it cannot kill all tumor cells. So, an isoform of
manganese superoxide dismutase isolated from a human liposarcoma cell line, obtained as
recombinant molecule (rMnSOD), which displayed oncotoxic action on cultured breast cancer cells
(Mancini et al.,2006), was used to treat human endometrial cancer cells. This enzyme catalizes the
dismutation of O2 – free radicals in H2O2, preventing the accumulation of ROS. H2O2 can be further
converted into H2O and O2 by catalase and ⁄or glutathione peroxidase. Once rMnSOD penetrates
cancer cells, it transforms free radicals into H2O2. This, in neoplastic cells, may lead to an high
accumulation of H2O2 that causes apoptosis of them, because of their lower level of catalase
(Mancini et al., 2008). We evaluated the effects of the rMnSOD treatment on cultured human
endometrial adenocarcinoma cell line HTB-112. We demonstrated the oncotoxic effect of this
protein, which lead HTB/112 cells to apoptotic death, by immunocytochemistry at light and
electron microscopy and by comet assay test, which shows early DNA damage induced by the
accumulation of H2O2.
References: Siegel CA 62, 10–29; 2012; Holland Clin Oncol 20:448-56 2008 ; Mancini Int J
Cancer, 119: 932–943¸ 2006.