Search Results (639)

Cancer therapy remains limited by drug resistance and poor selectivity, while inflammation-driven tumor progression further complicates treatment outcomes. Antimicrobial peptides (AMPs) have emerged as promising therapeutic alternatives due to their multifunctional properties. In this study, we investigated the anticancer and immunomodulatory activities of KI17, a rationally designed peptide derived from GL18, a peptide fragment identified from the talisin protein of Talisia esculenta. KI17 exhibited dose-dependent antiproliferative effects against murine and human melanoma (B16F10-Nex2, SK-MEL-2, A375) and cervical cancer (HeLa) cell lines, while displaying reduced cytotoxicity toward non-tumoral BV-2 microglial cells, resulting in a favorable selectivity index. Mechanistic analyses revealed that KI17 induces morphological alterations, mitochondrial dysfunction, caspase activation, and late-stage apoptosis, together with G0/G1 cell cycle arrest accompanied by accumulation of the Sub-G0 population, indicating coordinated regulation of cell death and cell cycle progression. KI17 effectively suppressed lipopolysaccharide (LPS)-induced microglial activation, markedly reducing pro-inflammatory cytokine and nitric oxide production without compromising cell viability. These biological activities are consistent with the peptide’s optimized physicochemical features, including increased cationicity, amphipathicity, and α-helical folding. Overall, our findings demonstrate that KI17 combines selective anticancer activity with potent immunomodulatory effects, highlighting its potential as a bioinspired peptide for further preclinical development in cancer therapy. Full article

Background/Objectives: Malignant melanoma is characterized by constitutive PI3K/Akt/mTOR and MAPK activation, driving aggressive behavior and therapeutic resistance. Alpha-lipoic acid (αLA), a naturally occurring dithiol compound with an established clinical safety profile, has shown anticancer potential; however, its integrated molecular mechanisms in melanoma remain poorly defined. This study aimed to comprehensively evaluate the cytotoxic and mechanistic effects of αLA in B16F10 murine melanoma cells. Methods: Antiproliferative effects were assessed by MTT assay at four concentrations (250, 500, 750, 1000 µM) over 48 h. Protein levels of apoptotic markers (Bax, Bcl-2, Caspase-3, AIF), kinase signaling components (p-Akt, p-mTOR, p-ERK, p-JNK), ER stress markers (GRP78, GADD153/CHOP), and cell cycle regulator Wee1 were quantified by ELISA at a specifically selected sub-lethal concentration of 750 µM (inducing ~38% growth inhibition). Results: αLA dose-dependently inhibited B16F10 proliferation. At 750 µM, it triggered robust intrinsic apoptotic signaling, evidenced by a nearly 10-fold shift in the Bax/Bcl-2 ratio and greater than 9-fold Caspase-3 activation. Elevated AIF suggested profound mitochondrial stress and the potential priming of concurrent caspase-independent cell death mechanisms. αLA suppressed survival signaling by reducing p-Akt (44%), p-mTOR, p-ERK, and p-JNK. Treatment triggered lethal ER stress via GRP78 and GADD153/CHOP upregulation and upregulated Wee1, suggesting the induction of stress-responsive checkpoint signaling. The simultaneous CHOP upregulation and p-Akt suppression highlight a concurrent dysregulation of stress and survival pathways, suggesting a potential pro-apoptotic interplay. Conclusions: αLA exerts potent multi-target anticancer effects by inducing a broad spectrum of associated molecular changes, including the suppression of PI3K/Akt/mTOR and MAPK networks, induction of ER stress, engagement of cell cycle checkpoints, and activation of the mitochondrial Bax/Bcl-2/Caspase-3 axis. Importantly, these correlative findings do not establish proven pathway dependencies. Nevertheless, this concurrent dysregulation positions αLA as a potential disruptor of inter-pathway resilience underlying drug resistance. Full article

Melanoma remains highly lethal with frequent resistance to current therapies. Here we identify a marine-derived cyclopentapeptide, turnagainolide B, as a potent anti-melanoma agent that selectively kills B16-F10 melanoma cells (IC₅₀ = 50 μM) with low toxicity to normal skin cells. Using bioassay-guided isolation, we also obtained a new analogue, turnagainolide H, and elucidated their structures and biosynthetic pathways. Mechanistically, turnagainolide B induces a previously undescribed “dual-hit” autophagic signature: it simultaneously promotes autophagy initiation (via PI3K/mTOR suppression, evidenced by ATG5 and LC3B-II upregulation) and blocks autophagic degradation (evidenced by p62 accumulation). Co-treatment with chloroquine partially rescued cell viability and decreased LC3B levels, confirming that cell death depends on active autophagic flux disruption. Transcriptomic analysis, together with AI target prediction and docking, identified PI3K as a potential direct target, with downregulation of PI3K, mTOR, and BNIP3 supporting an imbalanced autophagic state. In a syngeneic mouse melanoma model, turnagainolide B significantly suppressed tumor growth, reduced melanin content and Ki67 expression, and enhanced CD8⁺ T cell infiltration. Collectively, this work expands the chemical diversity of the turnagainolide family, uncovers a unique “dual-hit” autophagic mechanism, and establishes turnagainolide B as a promising lead for melanoma therapy. Full article

Immune checkpoint inhibitors (ICIs), comprising anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), anti-programmed cell death protein 1 (PD-1), and anti-programmed death-ligand 1 (PD-L1), have transformed melanoma therapy, yet the tumour microenvironment (TME), the pivotal biological interface where therapeutic efficacy, resistance, and toxicity are determined, remains incompletely characterized. This dual systematic review and meta-analysis (PROSPERO: CRD420261374242) followed PRISMA 2020 and included 58 preclinical (B16F10/C57BL/6; 46 quantitative) and 44 clinical studies (19 quantitative) to calculate pooled standardized mean differences (SMDs) for six intratumoral TME parameters. Checkpoint blockade consistently shifted the TME toward an immune-activated state, an effect that remained robust in sensitivity analyses despite substantial heterogeneity (I-squared heterogeneity statistic (I²) = 68–88%). Preclinically, ICIs significantly increased CD8⁺ T-cell infiltration (SMD = 1.45, p < 0.001), interferon-gamma (IFN-γ) (SMD = 1.78, p < 0.001), CD8/regulatory T-cell (Treg) ratio (SMD = 0.91, p = 0.005), and apoptosis (SMD = 3.54, p < 0.001) and reduced PD-L1 (SMD = −0.88, p = 0.004) and Ki-67 (SMD = −1.43, p = 0.028). Clinically, CD8⁺ infiltration and PD-L1 both increased (SMD = 0.72, p < 0.001; SMD = 0.67, p = 0.001), contrasting with the preclinical PD-L1 decrease. Meta-regression demonstrated superior anti-PD-L1 efficacy over CTLA-4 for effector parameters: IFN-γ +3.59 (p = 0.009), CD8/Treg +10.69 (p = 0.003), apoptosis +9.76 (p = 0.004), and Ki-67 −6.28 (p = 0.040). These findings establish the TME as a critical determinant of ICI outcomes, indicate that PD-L1 amplifies effector functions in the B16F10 model, and highlight translational gaps in TME reprogramming. Full article

Background: Photodynamic therapy (PDT) is a promising minimally invasive approach for melanoma; however, many photosensitizers lose activity in aqueous media due to aggregation-induced quenching effects. Objectives: The aim of this study was to develop and characterize castor oil–based nanoemulsions containing chlorophyll (NFs-Chl) and to evaluate their in vitro photodynamic potential against melanoma cells (B16-F10), as well as their selectivity compared with human keratinocytes (HaCaT). Methods: NFs-Chl were prepared by spontaneous emulsification. Physicochemical characterization was carried out using dynamic light scattering (DLS), UV–Vis spectroscopy, FTIR, and Raman spectroscopy. In vitro assays included MTT for cell viability (IC₅₀ determination), real-time cell proliferation (RealTime-Glo™), and cell migration analysis (scratch assay). All photodynamic treatments were performed under irradiation at 660 nm. Results: NFs-Chl exhibited homogeneous nanometric sizes (≈24–31 nm) and a low polydispersity index (≈0.25–0.40), indicating a narrow size distribution. UV–Vis spectra confirmed the preservation of the characteristic absorption peaks of chlorophyll after encapsulation. In B16-F10 cells, NFs-Chl associated with PDT significantly reduced cell viability and metabolic activity over 48 h. Furthermore, NFs-Chl inhibited the migratory capacity of B16-F10 cancer cells. Cell migration assays revealed a clear inhibition of B16-F10 cell migration following treatment with NFs-Chl + PDT. Conclusions: Encapsulation of chlorophyll into castor oil nanoemulsions protected the photosensitizer, improved its cellular delivery, and enhanced its photodynamic cytotoxic effect against melanoma cells, while relatively preserving normal keratinocytes in vitro. Full article

Melanoma exhibits pronounced metabolic plasticity and mitochondrial dependency, contributing to therapeutic resistance and tumor progression. Targeting mitochondrial function therefore represents a promising anticancer strategy. 2-Aminoethyl dihydrogen phosphate (2-AEH₂P), a bioactive phosphomonoester, has demonstrated antiproliferative potential, while metformin, a clinically established antidiabetic drug, acts as a mitochondrial complex I inhibitor and metabolic modulator. This study investigated the cytotoxic and mechanistic effects of 2-AEH₂P and metformin hydrochloride, individually and in combination, in human (SK-MEL-28) and murine (B16-F10) melanoma models, using non-tumorigenic fibroblasts (FN1 and L929) as controls. Cell viability, proliferation dynamics, cell-cycle distribution, mitochondrial membrane potential (ΔΨm), and apoptosis-associated markers were evaluated by flow cytometry. 2-AEH₂P reduced melanoma cell viability and proliferation while inducing G2/M accumulation, DNA fragmentation, mitochondrial depolarization, increased cytochrome c release, caspase-3 and caspase-8 activation, upregulation of p53 and Bad, and downregulation of Bcl-2. Metformin alone exerted moderate cytotoxic and pro-apoptotic effects. Notably, combined treatment markedly potentiated mitochondrial depolarization and intrinsic apoptotic signaling in melanoma cells, significantly lowering IC₅₀ values and enhancing caspase activation and cytochrome c release. Bliss independence analysis demonstrated synergistic interaction in SK-MEL-28 and B16-F10 cells. Although interaction scores indicated synergy in one fibroblast model, absolute cytotoxicity remained lower than in melanoma cells. These findings demonstrate that metabolic co-targeting with metformin enhances mitochondrial dysfunction-associated apoptotic signaling in melanoma cells, supporting a drug repositioning strategy aimed at exploiting mitochondrial vulnerability in metabolically adaptable tumors. Full article

Melanoma is a highly aggressive and metabolically adaptable cancer that often resists conventional therapies. Targeting core bioenergetic pathways may, therefore, represent an effective strategy to improve therapeutic responses, particularly in tumors dependent on mitochondrial function. SC18 is an imidazolidine-2,4-dione compound that binds the NADH-binding pocket of voltage-dependent anion channels (VDACs), inducing mitochondrial dysfunction. VDAC expression is increased in melanoma and strongly associated with advanced disease stage and poor prognosis. In this study, we evaluated the effects of SC18 in melanoma cell lines with distinct pigmentation states, including melanin-rich melanotic human MNT-1 and mouse B16-F1, as well as low/amelanotic human SKMel28 and mouse YUMM cells. VDAC1, VDAC2 and VDAC3 were highly expressed across these melanoma lines, all of which relied on both glycolysis and mitochondrial oxidative phosphorylation for ATP production. SC18 reduced mitochondrial membrane potential and oxygen consumption rates, accompanied by declines in intracellular ATP levels and TCA cycle substrate utilization. SC18 also increased reactive oxygen species, mitochondrial superoxide, and lipid peroxidation, indicating enhanced oxidative stress. These metabolic and redox disturbances were associated with reduced cell viability and significantly impaired migration in multiple melanoma cell lines, supporting a potential anti-metastatic effect. In addition, SC18 showed synergistic cytotoxicity when combined with other chemotherapeutic agents. Overall, SC18 disrupted mitochondrial metabolism, induced oxidative stress, and impaired survival and motility pathways, with more pronounced effects in low/amelanotic than in melanotic melanoma cells. Together, these findings support the further development of SC18 as a mitochondrial metabolic disruptor that targets redox vulnerabilities in melanoma. Full article

Microscale physical cues at the cell–extracellular matrix adhesion interface are increasingly being recognized as important regulators of cellular behavior. B16-F10 melanoma-derived cells retain melanogenic activity, including microphthalmia-associated transcription factor (MITF) expression and inducible melanin production, and are widely used for studies of melanogenesis and pigmentation-associated cellular responses. Melanocytic cells are sensitive to the physical characteristics of the surrounding microenvironment, including adhesion-dependent mechanical cues. However, the mechanism by which physical cues derived from the adhesion interface regulate melanoma cell function remains incompletely understood. In this study, we investigated the mechanism by which defined micropatterned substrates modulate melanoma cell morphology, migration, nuclear architecture, and melanogenic activity. Polydimethylsiloxane substrates with pillar- and hole-shaped microstructures (5, 10, and 50 µm diameters and spacings; 10 µm height or depth) were fabricated and coated with fibronectin. B16-F10 melanoma cells cultured on narrow pillar patterns (5 and 10 µm) exhibited restricted cell spreading, shortened protrusions, suppressed migration, and pronounced nuclear deformation compared with flat substrates. These mechanical constraints were accompanied by significant reductions in melanin production and downregulation of melanogenesis-related genes (Mitf, Tyr, and Tyrp1). Comparable trends were observed for Matrigel-coated substrates, indicating that microscale topography exerted consistent effects on B16-F10 melanoma cell responses across the tested extracellular matrix conditions. Collectively, our results demonstrate that surface topography with narrow pillar microstructures is associated with topography-dependent changes in cell behavior and melanogenic activity, providing insights into how microscale topographic confinement influences melanoma cell morphology and melanogenic activity. Full article

Plant-derived extracellular vesicles (PDEVs) are emerging as promising bioactive materials for biomedical and dermatological applications. In this study, we isolated and characterized exosome-like vesicles derived from Rosa damascena callus culture medium (RSC-EXO) and evaluated their molecular features and biological activities in skin-related cellular models. Nanoparticle tracking analysis and cryo-electron microscopy showed that RSC-EXO exhibited a nanoscale size distribution and spherical morphology. Western blotting confirmed enrichment of the plant EV-associated markers PEN1 and TET8. RSC-EXO were efficiently internalized by human dermal fibroblasts and showed markedly improved biocompatibility compared with crude conditioned medium (RSC-CM). Functionally, RSC-EXO significantly increased collagen synthesis and showed a trend toward enhanced wound closure in fibroblasts. In addition, RSC-EXO reduced melanin production in α-MSH-stimulated B16F10 melanoma cells and suppressed the secretion of pro-inflammatory cytokines, including IL-1α, IL-6, and TNF-α, in LPS-stimulated RAW 264.7 macrophages. Proteomic analysis revealed a distinct cargo enriched in stress-, defense-, and metabolism-related proteins, while small RNA sequencing identified a heterogeneous small RNA population containing a limited fraction of miRNA-sized reads. Collectively, these findings suggest that RSC-EXO represents a biologically active plant-derived vesicle population with regenerative and anti-inflammatory activity observed in vitro in skin-related cellular models and support its potential as a promising platform for future cosmeceutical and dermatological applications. Full article

Background/Objectives: Photodynamic therapy (PDT) is severely limited by the hypoxic tumor microenvironment, which restricts reactive oxygen species (ROS) generation and compromises therapeutic efficacy. To address this critical barrier, we engineered a multifunctional nanocomposite (Pha@FSMP) integrating oxygen supplementation, pH-responsive drug release, and magnetic targeting for enhanced PDT. Methods: The platform is constructed with a superparamagnetic Fe₃O₄ core, coated in amino-functionalized mesoporous silica (mSiO₂) loaded with MnO₂ as an oxygen-evolving catalyst, and surface-conjugated with the pH-responsive copolymer PEG-b-PAsp to encapsulate the hydrophobic photosensitizer Pha. We characterized its core physicochemical and functional properties, and evaluated its photodynamic efficacy via in vitro cellular assays and in vivo studies in a murine melanoma model. Results: In vitro assays demonstrated significant elevation of intracellular ROS levels and enhanced PDT-mediated cytotoxicity against B16-F10 melanoma cells. In vivo studies in a murine melanoma model confirmed potent tumor growth inhibition, metastasis suppression, and prolonged survival, accompanied by excellent biosafety. Conclusions: Collectively, this oxygen-augmented nanocomposite represents a promising strategy to overcome hypoxia-associated PDT resistance, offering a translatable platform for improved cancer therapy. Full article

This study reports the synthesis, characterization, DFT calculations and in vitro antimicrobial, cytotoxic and antiproliferative evaluation of La(III), Eu(III), and Gd(III) metal complexes with ampicillin. The compounds were characterized by Thermal Gravimetric Analysis (TGA), elemental analysis, ultraviolet–visible spectroscopy (UV–Vis), Fourier-transform infrared spectroscopy (FTIR), and proton nuclear magnetic resonance (¹H NMR), indicating a 2:1 metal-to-ligand ratio with ampicillin, and likely, a coordination through carbonyl, carboxylic and β-lactam groups, with the general formula [Ln₂(L)(Cl)₅(H₂O)_x] (Ln = La(III), Eu (III), Gd (III), and x = 2 for La(III), 5 for Eu(III) and Gd(III), L-ampicillin anion). Antimicrobial studies showed activity against ampicillin-resistant Staphylococcus aureus (MIC = 15.6 µg·mL⁻¹) but no activity against Escherichia coli. In cytotoxicity studies, all complexes inhibited B16-F10 (murine melanoma) proliferation, with GI₅₀ values around 140 µg·mL⁻¹. Against U251 (glioma) cell line, only [Eu₂(L)(Cl)₅(H₂O)₅] exhibited cytotoxicity activity, GI₅₀ = 104 µg·mL⁻¹, and notably, [Eu₂(L)(Cl)₅(H₂O)₅] was active against MCF7 (breast carcinoma) with a GI₅₀ = 8.1 µg·mL⁻¹. However, all complexes exhibited high cytotoxicity in NIH-3T3 cells (GI₅₀ = 0.030–2.90 µg·mL⁻¹), indicating limited selectivity between normal and cancer cells. Nevertheless, except for the La complex, most compounds were less cytotoxic than doxorubicin, highlighting the need for further optimization to improve selectivity. Full article

The aim of this study was to investigate the anti-melanogenic effects and underlying mechanisms of PFRMY (Pro-Phe-Arg-Met-Tyr), a pentapeptide derived from tilapia skin (Oreochromis niloticus), using B16F10 murine melanoma cells. Treatment with PFRMY (1.0 mg/mL) significantly reduced intracellular melanin content and tyrosinase (TYR) activity by 39.55 ± 1.51% and 32.46 ± 1.31%, respectively. RT-PCR and Western blotting analyses revealed that PFRMY suppressed melanogenesis through the α-MSH/PKA/CREB signaling pathway. Notably, PFRMY reversed α-MSH-induced upregulation of key downstream factors including PKA, CREB, MITF, and TYR, while showing minimal effects on the protein expression of MC1R or α-MSH. Molecular docking further suggested that PFRMY binds to MC1R with higher affinity than α-MSH, potentially occupying the ligand-binding site and thereby interfering with downstream signaling. Collectively, these findings demonstrate that PFRMY effectively inhibits melanogenesis by competitively antagonizing the α-MSH/MC1R axis, highlighting its potential as a safe and efficacious ingredient for hyperpigmentation treatment and cosmetic applications. Full article

Tyrosinase promotes excessive deposition of melanin, which may lead to severe skin diseases. Passiflora edulis f. edulis seeds have been reported to be rich in diverse bioactive constituents exhibiting potential tyrosinase inhibitory activity. However, the principal bioactive constituents responsible for tyrosinase inhibitory activity and its underlying mechanisms remain largely unclear. Therefore, this study aimed to: (1) optimize SC-CO₂ extraction of Passiflora edulis f. edulis seed oil (PFSO) for maximum yield and bioactive preservation; (2) comprehensively characterize its physicochemical and phytochemical profile; (3) elucidate the tyrosinase inhibition mechanism through kinetic, spectroscopic, and computational approaches; and (4) validate its safety, antioxidant, and anti-pigmentation efficacy in a zebrafish model. PFSO exhibited a yield of 24.96%, with a high content of unsaturated fatty acids (88.03%, mainly linoleic acid at 74.40%). The oil inhibited tyrosinase via a reversible mixed-type mechanism (IC₅₀ = 1.12 mg/mL). Fluorescence spectroscopy and molecular docking revealed that linoleic acid binds to LYS180 and β-sitosterol binds to TYR78, mainly driven by hydrogen bonding and hydrophobic interaction, which changed the microenvironment of tryptophan residues and indicated static quenching. Further validation experiments revealed that the major constituent, linoleic acid, exhibited only weak inhibitory activity against tyrosinase (IC₅₀ = 29.44 mg/mL), whereas the key component β-sitosterol markedly suppressed tyrosinase activity (IC₅₀ = 46.43 μg/mL). In vitro assays demonstrated PFSO’s significant efficacy in reducing the melanin content and tyrosinase activity in α-MSH-stimulated B16F10 murine melanoma cells. In vivo experiments in zebrafish that received dietary supplementation with PFSO confirmed that PFSO (≤5 mg/mL) reduced ROS production, suppressed melanin deposition, inhibited tyrosinase activity, and downregulated the expression of melanogenesis-related genes (TYR, TYRP1, TYRP2, MITF). This study provides, for the first time, a comprehensive elucidation of PFSO’s potential as a natural tyrosinase inhibitor, integrating extraction optimization, multicomponent characterization, multimodal inhibition analysis, and in vivo validation. Full article

The aim of this study was to investigate which physicochemical and structural properties of cationic peptides P1–P6 may determine their selective anticancer activity against melanoma cells and their interactions with tumor cell membranes. An integrated approach was applied, including characterization in solution (osmotic pressure, NaCl stability, surface tension); cytotoxicity evaluation against Me45, B16F10, and HaCaT cells; analysis of interactions with phosphatidylglycerol (POPG) model membranes using isothermal titration calorimetry and steady-state fluorescence spectroscopy; membrane permeability assays; and F-actin staining. Anticancer activity depended on positively charged residues, hydrophobic amino acids, and sequence arrangement. Tryptophan-rich peptides P2 and P5 exhibited strong membrane interactions and high efficacy after 72 h. Highly hydrophobic P4, containing long C₁₂ chains with a relatively low net charge, caused nonselective lysis. P3 showed reduced activity due to insufficient amphipathicity, whereas P6, with excessive WWW and KKKK motifs, exhibited weak or nonselective effects. Thermodynamic and fluorescence analyses indicated that P2 and P5 initially bind POPG membranes via entropy-driven electrostatic interactions, followed by hydrophobic insertion of tryptophan residues, evidenced by increased fluorescence intensity and a blue shift of the emission maximum. P2, P4, and P5 induced actin cytoskeleton reorganization and increased membrane permeability, emphasizing the role of balanced amphipathicity and charge–hydrophobicity in designing selective anticancer peptides. Full article

Background: Melanoma is one of the most dangerous types of skin cancer, with its global incidence having surged in recent years. There exists an urgent clinical need for novel therapeutic strategies that combine high efficacy, low toxicity, and multiple mechanisms of action. Methods: This study applies a “Property Optimization and Therapeutic Synergy” strategy, selecting the natural active polysaccharide component, Cordyceps polysaccharides (WCP), as a functional carrier to encapsulate the broad-spectrum chemotherapeutic agent, 10-Hydroxycamptothecin (10HCPT, HCPT). Leveraging non-covalent interactions between the two components, a self-assembly nanoscale drug delivery system (H-W NPs) with high stability and dual antitumor activity was constructed to achieve more efficient and precise antitumor effects. Results: The H-W NPs demonstrated outstanding antitumor efficacy both in vitro and in vivo. The H-W NPs achieved a threefold increase in the inhibition rate against B16-F10 cells compared to free HCPT in vitro and demonstrated a remarkable tumor inhibition rate of 95.08% in vivo. The therapeutic effect may be attributed to the dual antitumor mechanisms of the H-W NPs. Mechanistic studies revealed a synergistic dual-mode of action driving this potent efficacy. Firstly, H-W NPs efficiently induced caspase-3-mediated apoptosis in tumor cells. RNA sequencing analysis suggested the involvement of pathways related to cell cycle arrest and apoptosis. Additionally, H-W NPs promoted the expansion and activation of CD8⁺ T cells in the spleen. These activated cytotoxic T cells reinforced the apoptotic cascade, effectively amplifying the caspase-3-mediated death signal. Conclusions: In summary, the self-assembly nanoscale drug system achieved potent antitumor efficacy through the synergistic action of direct tumor cell killing and immune modulation, offering a highly promising strategy for the development of novel formulations against melanoma. Full article