Combination of chemotherapy and physical plasma elicits melanoma cell death via upregulation of SLC22A16

Sagwal, Sanjeev Kumar; Pasqual-Melo, Gabriella; Bodnar, Yana; Gandhirajan, Rajesh Kumar; Bekeschus, Sander

doi:10.1038/s41419-018-1221-6

Cited by 91 publications

(71 citation statements)

References 76 publications

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“…Nevertheless, in metastatic colon cancer patients treated with oxaliplatin-based chemotherapy, the presence of a mutated TLR4 allele is correlated with a significant decrease in progression-free and overall survival [33]. Additionally, oxaliplatin has been shown to induce CXCL10 secretion by melanoma cells, another ICD feature [80].…”

Section: Direct Effectsmentioning

confidence: 99%

Platinum Derivatives Effects on Anticancer Immune Response

et al. 2019

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Along with surgery and radiotherapy, chemotherapeutic agents belong to the therapeutic arsenal in cancer treatment. In addition to their direct cytotoxic effects, these agents also impact the host immune system, which might enhance or counteract their antitumor activity. The platinum derivative compounds family, mainly composed of carboplatin, cisplatin and oxaliplatin, belongs to the chemotherapeutical arsenal used in numerous cancer types. Here, we will focus on the effects of these molecules on antitumor immune response. These compounds can induce or not immunogenic cell death (ICD), and some strategies have been found to induce or further enhance it. They also regulate immune cells' fate. Platinum derivatives can lead to their activation. Additionally, they can also dampen immune cells by selective killing or inhibiting their activity, particularly by modulating immune checkpoints' expression.Cell death is characterized by morphological alterations that have been historically used by The Nomenclature Committee on Cell Death (NCCD) to classify this cellular process into three different forms: type I or apoptosis, type II or autophagy, and type III or necrosis. Although limited, this morphological classification remains widely used, independently of essential molecular aspects of the cell death process. New NCCD classifications focus on molecular mechanisms and on the biochemistry of intracellular signalization effectors. Currently, it is clear that connections and overlaps exist between the different types of cell death. The majority of chemotherapeutic drugs are known to induce apoptosis or necrosis. Engagement of a particular type of cell death depends on the stress type, interaction between induction factors, genetic cell background, organelle content and enzymatic proteins arsenal [3,4].The action of chemotherapy relies not only on its cytotoxic effect on cancer cells, but also on its ability to affect immune cells.

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Section: Direct Effectsmentioning

confidence: 99%

Platinum Derivatives Effects on Anticancer Immune Response

et al. 2019

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“…Medical gas plasma technology recently gained attention due to its antitumor activity against many types of cancers [4][5][6]. Specifically, plasma was shown to inactivate, for instance, malignant melanoma [7], squamous cell carcinoma [5,8], lung cancer [9], colon cancer [10], pancreatic cancer [11], osteosarcoma [12], glioblastoma [13], and hepatocellular carcinoma [14].…”

Section: Introductionmentioning

confidence: 99%

Gas Plasma-Treated Prostate Cancer Cells Augment Myeloid Cell Activity and Cytotoxicity

et al. 2020

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Despite recent improvements in cancer treatment, with many of them being related to foster antitumor immunity, tumor-related deaths continue to be high. Novel avenues are needed to complement existing therapeutic strategies in oncology. Medical gas plasma technology recently gained attention due to its antitumor activity. Gas plasmas act via the local deposition of a plethora of reactive oxygen species (ROS) that promote the oxidative cancer cell death. The immunological consequences of plasma-mediated tumor cell death are only poorly understood, however. To this end, we exposed two prostate cancer cell lines (LNCaP, PC3) to gas plasma in vitro, and investigated the immunomodulatory effects of the supernatants in as well as of direct co-culturing with two human myeloid cell lines (THP-1, HL-60). After identifying the cytotoxic action of the kINPen plasma jet, the supernatants of plasma-treated prostate cancer cells modulated myeloid cell-related mitochondrial ROS production and their metabolic activity, proliferation, surface marker expression, and cytokine release. Direct co-culture amplified differentiation-like surface marker expression in myeloid cells and promoted their antitumor-toxicity in the gas plasma over the untreated control conditions. The results suggest that gas plasma-derived ROS not only promote prostate cancer cell death but also augment myeloid cell activity and cytotoxicity.

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“…High species concentrations can be used to exploit apoptotic redox signaling pathways in tumor cells [29], and first cancer patients have benefited from plasma therapy [30]. Plasma treatment can act in concert with other drugs [31][32][33], and plasma-generated reactive species induce pro-immunogenic molecules on tumor cells, such as ecto-calreticulin (CRT) [34][35][36]. Although the release of this and other DAMP signals after plasma treatment in melanoma cells has been shown, evidence of immune cell activation in response to plasma-treated melanoma is scarce.…”

Section: Introductionmentioning

confidence: 99%

Activation of Murine Immune Cells upon Co-culture with Plasma-treated B16F10 Melanoma Cells

et al. 2019

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Recent advances in melanoma therapy increased median survival in patients. However, death rates are still high, motivating the need of novel avenues in melanoma treatment. Cold physical plasma expels a cocktail of reactive species that have been suggested for cancer treatment. High species concentrations can be used to exploit apoptotic redox signaling pathways in tumor cells. Moreover, an immune-stimulatory role of plasma treatment, as well as plasma-killed tumor cells, was recently proposed, but studies using primary immune cells are scarce. To this end, we investigated the role of plasma-treated murine B16F10 melanoma cells in modulating murine immune cells’ activation and marker profile. Melanoma cells exposed to plasma showed reduced metabolic and migratory activity, and an increased release of danger signals (ATP, CXCL1). This led to an altered cytokine profile with interleukin-1β (IL-1β) and CCL4 being significantly increased in plasma-treated mono- and co-cultures with immune cells. In T cells, plasma-treated melanoma cells induced extracellular signal-regulated Kinase (ERK) phosphorylation and increased CD28 expression, suggesting their activation. In monocytes, CD115 expression was elevated as a marker for activation. In summary, here we provide proof of concept that plasma-killed tumor cells are recognized immunologically, and that plasma exerts stimulating effects on immune cells alone.

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Combination of chemotherapy and physical plasma elicits melanoma cell death via upregulation of SLC22A16

Cited by 91 publications

References 76 publications

Platinum Derivatives Effects on Anticancer Immune Response

Platinum Derivatives Effects on Anticancer Immune Response

Gas Plasma-Treated Prostate Cancer Cells Augment Myeloid Cell Activity and Cytotoxicity

Activation of Murine Immune Cells upon Co-culture with Plasma-treated B16F10 Melanoma Cells

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