Abstract
Photodynamic therapy (PDT) is a promising therapeutic modality for treating cancer, including breast tumors. The oxidative damage caused by PDT culminates in cell death, induction of immune response, and the resulting destruction of the tumor. This study aimed to evaluate the gene expression profiling of genes BCL-2, BAX, and HER-2 and their proteins after PDT, associating it with the necrosis caused by this therapy under different fluences. Twenty-eight female rats received a single dose of 7,12-dimethylbenz (a) anthracene (DMBA - 80mg/kg), by gavage, for breast tumor induction. After the tumors grew, the animals were divided into four groups: G1 - control group – untreated breast tumor – and G2, G3, and G4 groups treated with PDT using Photogem@ as photosensitizer and interstitial irradiation, with fluences of 50J/cm, 100J/cm, and 150J/cm, respectively. Samples of tumors were harvested for histological examination by RT-qPCR. The RT-qPCR showed that the gene expression profiling of BCL-2, BAX, and HER-2 was not altered after PDT. Hemorrhagic necrosis and qualitatively greater vascular and cellular damage were observed and correlated positively with the fluence. PDT does not seem to induce the modulation of genes related to apoptosis. The results indicate that the type of cell death stimulated by PDT in breast tumor is necrosis.
Highlights
Photodynamic therapy (PDT) is a promising therapeutic modality used for the treatment of cancer and other ailments
Comparing the fluences and the depth of the breast tissue necrosis, this study revealed that the higher the fluence, the greater is the area of necrosis and vascular injury
PDT does not seem to induce the modulation of genes related to apoptosis under the irradiation parameters used with Photogem and analyzed after 30h of therapy
Summary
Photodynamic therapy (PDT) is a promising therapeutic modality used for the treatment of cancer and other ailments.The induction of oxidative stress and formation of reactive oxygen species (ROS) result in organelle damage, culminating in cell death and destruction of the tumor or abnormal tissue after PDT (Oleinick & Evans, 1998). Photodynamic therapy (PDT) is a promising therapeutic modality used for the treatment of cancer and other ailments. Apoptosis is a common mechanism of cell death in this case; the triggering events responsible for the PDT-mediated apoptotic response are not clear. Understanding the mechanisms involved in PDT-induced apoptosis may improve therapeutic efficacy (Srivastava et al 2001), contributing to the knowledge on treatment failures (Itoh et al 2000; Senderowicz, 2004). PDT could be used as an alternative treatment for the control of tumor growth or as an adjunct therapy to surgery, in order to avoid recurrence. The downregulation of Bcl-2 and related proteins may result in triggering apoptosis (Srivastava et al 2001; Kessel & Arroyo, 2007)
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