Abstract LB-169: Sulfasalazine sensitizes glioblastoma cells to radiation treatment

• Published in: Cancer research (Chicago, Ill.) Vol. 70; no. 8_Supplement; p. LB-169
• Main Authors: Sleire, Linda, Wang, Jian, Heggdal, Jan, Pedersen, Paal-Henning, Enger, Per Øyvind
• Format: Journal Article
• Language: English
• Published: 15.04.2010
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM10-LB-169

Abstract Glioblastomas (GBMs) are lethal cancers with a limited response to ionizing radiation. Recent studies suggest that Sulfasalazine (SAS), a drug used to treat inflammatory bowel disease, inhibits the xCT antiporter system in glioma cells, thereby blocking their uptake of cystine. Since the availability of cystine is a rate limiting step in intracellular antioxidant production, we wanted to investigate whether sulfasalazine sensitizes glioma cells to radiation. SAS effect on glioma cell growth was investigated using a electric cell substrate impedance sensing (ECIS) instrument. All cell lines showed altered growth curves in response to SAS treatment. Further, U251 glioma cells were treated with escalating doses of SAS, alone or in combination with radiation (8 Gy). Immunocytochemistry for the apoptotic marker Annexin V as well as DAPI staining to assess nuclear integrity were conducted to estimate cell death following treatment. All treatment groups exhibited increased rates of cell death compared to untreated controls. However, a combination of SAS and radiation resulted in higher levels of cell death, than radiation or SAS administered alone. In order to assess whether this can be exploited therapeutically, we are currently preparing to treat nude rats harbouring gliblastoma biopsy xenografts with SAS, alone or in combination with radiation. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-169.