1,720,995 research outputs found
PDT and antitumor immunity: the beginnings of the story
This mini-review reports a brief description of the first experiments conducted by Canti’s group on the role of photodynamic therapy in generating immunity against cancer. It highlights for the first time the effective role of PDT in the induction of anti-tumor T lymphocytes and shows that this effect is tumor-specific. It has also been reported how this adoptive immunity can improve the efficacy of chemotherapy. These studies have helped to open an important new field of scientific research on the role of PDT-generated immunity and to stimulate today’s important new pre-clinical approaches. Graphical abstract: (Figure presented.
Role of RKIP in the tumor response to photooxidative damage
The Raf-kinase inhibitor protein (RKIP) plays a role in the regulation of different processes, through its interaction with several signaling pathways. These pathways include the mitogen activated protein kinase (MAPK), nuclear factor kappa-light chain enhancer of activated B cells (NF-κB), G protein-coupled receptors (GPCR) and glycogen synthase kinase 3 beta (GSK 3β). RKIP negatively affects tumor survival and proliferation, acting as a metastasis suppressor. Moreover, RKIP overexpression has been reported to reverse tumor chemo/immuno/radio-resistance and support the anticancer host immuno-surveillance. The aim of this work is to evaluate the role of RKIP in cancer cells during a photooxidative damage induced by photodynamic therapy (PDT). PDT treatment is based on three components: a photosensitizer, light and oxygen. Their combined action produces singlet oxygen (1O2) and/or reactive oxygen species (ROS) leading to an oxidative insult in tumor cells. Dependently on the PDT dose, the response of tumor cells can have a double outcome: stimulation of tumor cell proliferation with a low PDT dose (IC50), or tumor growth arrest in the case of a high PDT dose (IC50). We evaluated RKIP expression within its complex network, correlating with other factors involved in the tumor response to oxidative stress. We found a link between the expression of RKIP and NF-κB, MAPK, Snail and Nrf2 according to the type of the oxidative insult. In the presence of low PDT, RKIP is downregulated, while NF-κB, Snail and Nrf2 are upregulated: an expression profile that stimulates tumor proliferation and resistance. Conversely, RKIP is overexpressed in the case of high PDT, thus allowing an arrest of tumor growth.Considering that many antitumor drugs develop ROS/RNS causing disease recurrence and drug resistance, RKIP could be a good prognostic marker to follow patients' response to anticancer therapies
The ROS-KRAS-Nrf2 axis in the control of the redox homeostasis and the intersection with survival-apoptosis pathways: Implications for photodynamic therapy
Bystander effect in photosensitized prostate cancer cells with a different grade of malignancy: The role of nitric oxide
Photodynamic therapy (PDT) is a therapeutic modality based on the simultaneous action of three elements: photosensitizer, light and oxygen. This triad generates singlet oxygen and reactive oxygen species that can reduce the mass of a tumor. PDT is also able to stimulate iNOS, the enzyme that generates nitric oxide (NO). The role of NO in PDT-treated cancer cells has been investigated in several studies. They showed that low iNOS/NO levels stimulate signaling pathways that promote tumor survival, while high iNOS/NO levels arrest tumor growth. There is increasing evidence that ROS/RNS control both proliferation and migration of cells in the vicinity of PDT-treated tumor cells (so-called bystander cells). In this work, we addressed the question of how NO, which is generated by weak PDT, affects bystander cells. We used a conditioned medium: medium of PDT-treated tumor cells containing the stressors produced by the cells was added to untreated cells mimicking the neighboring bystander cells to investigate whether the conditioned medium affects cell proliferation. We found that low-level NO in prostate cancer cells affects the bystander tumor cells in a manner that depends on their malignancy grade
Effects of prolonged treatment with decarbazine on tumor metastatic potentialin mice bearing Lewis lung carcinoma.
Effects of melatonin on doxorubicin cytotoxicity in sensitive and pleiotropically resistant tumor cells.
Seasonal dependency of the effects of experimental stressors on tumor metastasis in ice bearing Lewis lung carcinoma
Small Interfering RNA-Mediated Silencing of Glutathione-S-transferase A1 Sensitizes Hepatic Carcinoma Cells to Photodynamic Therapy with Pentaphyrins
Photodynamic therapy (PDT) uses nontoxic photosensitizers and visible light to produce reactive oxygen species that kill malignant cells by apoptosis or necrosis. Silencing the antioxidant GSTA1-1 gene by siRNA sensitizes hepatic HepG2 cells to PDT with pentaphyrins. The study is a proof-of-concept for combining PDT with antigene molecules that decrease cellular response to oxidative stress
Is haem the real target of COVID-19?
Although a vaccination campaign has been launched in many countries, the COVID-19 pandemic is not under control. The main concern is the emergence of new variants of SARS-CoV-2; therefore, it is important to find approaches to prevent or reduce the virulence and pathogenicity of the virus. Currently, the mechanism of action of SARS-CoV-2 is not fully understood. Considering the clinical effects that occur during the disease, attacking the human respiratory and hematopoietic systems, and the changes in biochemical parameters (including decreases in haemoglobin [Hb] levels and increases in serum ferritin), it is clear that iron metabolism is involved. SARS-CoV-2 induces haemolysis and interacts with Hb molecules via ACE2, CD147, CD26, and other receptors located on erythrocytes and/or blood cell precursors that produce dysfunctional Hb. A molecular docking study has reported a potential link between the virus and the beta chain of haemoglobin and attack on haem. Considering that haem is involved in miRNA processing by binding to the DGCR8-DROSHA complex, we hypothesised that the virus may check this mechanism and thwart the antiviral response
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