In vitro efficiency and mechanistic role of indocyanine green as photodynamic therapy agent for human melanoma

2009 ◽  
Vol 6 (2) ◽  
pp. 105-116 ◽  
Author(s):  
Abdel-Megid Mamoon ◽  
Amira M. Gamal–Eldeen ◽  
Meghan E. Ruppel ◽  
Randy J. Smith ◽  
Thomas Tsang ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Indocyanine Green ◽  
Human Melanoma

scholarly journals Impact of Quantum Dot Surface on Complex Formation with Chlorin e6 and Photodynamic Therapy

Nanomaterials ◽  
2018 ◽  
Vol 9 (1) ◽  
pp. 9 ◽  
Author(s):  
Artiom Skripka ◽  
Dominyka Dapkute ◽  
Jurga Valanciunaite ◽  
Vitalijus Karabanovas ◽  
Ricardas Rotomskis
Keyword(s):  
Photodynamic Therapy ◽  
Cancer Therapy ◽  
Complex Formation ◽  
Chemical Properties ◽  
Disease Diagnosis ◽  
Chlorin E6 ◽  
Deep Tissue ◽  
Physico Chemical

Nanomaterials have permeated various fields of scientific research, including that of biomedicine, as alternatives for disease diagnosis and therapy. Among different structures, quantum dots (QDs) have distinctive physico-chemical properties sought after in cancer research and eradication. Within the context of cancer therapy, QDs serve the role of transporters and energy donors to photodynamic therapy (PDT) drugs, extending the applicability and efficiency of classic PDT. In contrast to conventional PDT agents, QDs’ surface can be designed to promote cellular targeting and internalization, while their spectral properties enable better light harvesting and deep-tissue use. Here, we investigate the possibility of complex formation between different amphiphilic coating bearing QDs and photosensitizer chlorin e6 (Ce6). We show that complex formation dynamics are dependent on the type of coating—phospholipids or amphiphilic polymers—as well as on the surface charge of QDs. Förster’s resonant energy transfer occurred in every complex studied, confirming the possibility of indirect Ce6 excitation. Nonetheless, in vitro PDT activity was restricted only to negative charge bearing QD-Ce6 complexes, correlating with better accumulation in cancer cells. Overall, these findings help to better design such and similar complexes, as gained insights can be straightforwardly translated to other types of nanostructures—expanding the palette of possible therapeutic agents for cancer therapy.

scholarly journals p32 promotes melanoma progression and metastasis by targeting EMT markers, Akt/PKB pathway, and tumor microenvironment

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Sunita Sinha ◽  
Satyendra Kumar Singh ◽  
Nitish Jangde ◽  
Rashmi Ray ◽  
Vivek Rai
Keyword(s):  
Tumor Microenvironment ◽  
Human Melanoma ◽  
Migration And Invasion ◽  
Therapy Failure ◽  
Melanoma Tumor ◽  
Melanoma Progression ◽  
Emt Markers

AbstractMelanoma originates from melanin-producing cells called melanocytes. Melanoma poses a great risk because of its rapid ability to spread and invade new organs. Cellular metastasis involves alteration in the gene expression profile and their transformation from epithelial to mesenchymal state. Despite of several advances, metastatic melanoma being a key cause of therapy failure and mortality remains poorly understood. p32 has been found to be involved in various physiological and pathophysiological conditions. However, the role of p32 in melanoma progression and metastasis remains underexplored. Here, we identify the role of p32 in the malignancy of both murine and human melanoma. p32 knockdown leads to reduced cell proliferation, migration, and invasion in murine and human melanoma cells. Furthermore, p32 promotes in vitro tumorigenesis, inducing oncogenes and EMT markers. Mechanistically, we show p32 regulates tumorigenic and metastatic properties through the Akt/PKB signaling pathway in both murine and human melanoma. Furthermore, p32 silencing attenuates melanoma tumor progression and lung metastasis in vivo, modulating the tumor microenvironment by inhibiting the angiogenesis, infiltration of macrophages, and leukocytes in mice. Taken together, our findings identify that p32 drives melanoma progression, metastasis, and regulates the tumor microenvironment. p32 can be a target of a novel therapeutic approach in the regulation of melanoma progression and metastasis.

In-vitro efficacy of indocyanine green-mediated photodynamic therapy in combination with cisplatin or etoposide

2015 ◽  
Vol 4 (4) ◽  
Author(s):  
Kamola Kasimova ◽  
Lothar Lilge ◽  
Brian C. Wilson
Keyword(s):  
Photodynamic Therapy ◽  
Indocyanine Green ◽  
Tumor Cells ◽  
Near Infrared ◽  
Lung Tumor ◽  
Infrared Light ◽  
Cancer Therapies ◽  
Cytotoxic Effects ◽  
Limited Efficacy

Abstract:Localizing the cytotoxic effects of cancer therapies to only affect the tumor cells is a goal in oncology, to maximize efficacy and minimize treatment-related morbidities. Most effective chemotherapeutic drugs have significant side effects due to off-target toxicity. By comparison, photodynamic therapy (PDT) is a localized therapy without significant systemic toxicity but may have limited efficacy. Hence, combining PDT with chemotherapy was investigated to determine if the anti-tumor effect of the latter could be enhanced. PDT using indocyanine green (ICG), activated by near-infrared light, was investigated in lung tumor cells

scholarly journals Role of Flavonoids in the Prevention of AhR-Dependent Resistance During Treatment with BRAF Inhibitors

2020 ◽  
Vol 21 (14) ◽  
pp. 5025
Author(s):  
Héloïse M. Leclair ◽  
Nina Tardif ◽  
Anaïs Paris ◽  
Marie-Dominique Galibert ◽  
Sébastien Corre
Keyword(s):  
Cell Lines ◽  
Melanoma Cell ◽  
Therapeutic Potential ◽  
Progression Free Survival ◽  
Human Melanoma ◽  
Human Melanoma Cell ◽  
Melanoma Cell Lines

BRAF and MEK inhibitors (BRAFi and MEKi) are the standard of care for the treatment of metastatic melanoma in patients with BRAFV600E mutations, greatly improving progression-free survival. However, the acquisition of resistance to BRAFi and MEKi remains a difficult clinical challenge, with limited therapeutic options available for these patients. Here, we investigated the therapeutic potential of natural flavonoids as specific AhR (Aryl hydrocarbon Receptor) transcription factor antagonists in combination with BRAFi. Experimental Design: Experiments were performed in vitro and in vivo with various human melanoma cell lines (mutated for BRAFV600E) sensitive or resistant to BRAFi. We evaluated the role of various flavonoids on cell sensitivity to BRAFi and their ability to counteract resistance and the invasive phenotype of melanoma. Results: Flavonoids were highly effective in potentiating BRAFi therapy in human melanoma cell lines by increasing sensitivity and delaying the pool of resistant cells that arise during treatment. As AhR antagonists, flavonoids counteracted a gene expression program associated with the acquisition of resistance and phenotype switching that leads to an invasive and EMT-like phenotype. Conclusions: The use of natural flavonoids opens new therapeutic opportunities for the treatment of patients with BRAF-resistant disease.

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