Unraveling the human protein atlas of metastatic melanoma in the course of ultraviolet radiation-derived photo-therapy

Konstantakou, Eumorphia G.; Velentzas, Athanassios D.; Anagnostopoulos, Athanasios K.; Giannopoulou, Aikaterini F.; Anastasiadou, Ema; Papassideri, Issidora S.; Voutsinas, Gerassimos E.; Tsangaris, George Th.; Stravopodis, Dimitrios J.

doi:10.1016/j.jprot.2017.11.015

Cited by 4 publications

(4 citation statements)

References 177 publications

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“…This strategy was effective at inhibiting both primary tumor growth and metastasis in a mouse model of melanoma, while it also complemented anti-melanoma activity of anti-PD1 immunotherapy [154]. Both UVB and UVC have also been shown to increase MLKL protein level [70], and vapor nanobubble photoporation-mediated delivery of MLKL protein to melanoma cells effectively induced necroptosis [155].…”

Section: Necroptosis In Melanomamentioning

confidence: 91%

“…In addition, exposure to ultraviolet A (UVA) upregulated p62/SQSTM1 and triggered p62-dependent response that involved nuclear factor erythroid 2-related factor 2 (NRF-2 encoded by NFE2L2) activity to counteract oxidative stress [68], while simulated sunlight irradiation was associated with induction of mitophagy [69]. In turn, low efficiency of autophagy execution promoted survival of melanoma cells exposed to UV irradiation [70]. On the contrary, others have demonstrated that loss of ATG7 in a BRAF V600E /PTEN null model of melanoma was associated with increased oxidative stress and senescence that prevented melanoma tumorigenesis [71], suggesting that inhibition of autophagy may also play a tumor-suppressing role.…”

Section: Autophagy In Melanomamentioning

confidence: 99%

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Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

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Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAF mut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

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Section: Necroptosis In Melanomamentioning

confidence: 91%

Section: Autophagy In Melanomamentioning

confidence: 99%

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

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“…Protocols for LC-MS/MS analysis were performed as previously described [ 35 , 48 , 49 ]. Briefly, each tryptic peptide mixture was separated in a linear gradient of 2–30% solution containing 99.9% acetonitrile and 0.1% formic acid, at a flow rate of 300 nL/min, on a C-18 column (75 μm × 50 cm, 100 Å, 2 μm bead-packed Acclaim Pepmap RSLC; Thermo Fischer Scientific, Waltham, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Technical protocols were employed as previously described [35,48]. Briefly, cell pellets derived from~10 7 cultured cells were suspended in lysis buffer containing 1.5 M Tris-HCl (pH 7.6), 3.5 M urea, 0.1 M SDS, and 3.2 mM DTE, and they were disrupted by tip sonication.…”

Section: Protein Extraction-tryptic Peptide Generationmentioning

confidence: 99%

From Proteomic Mapping to Invasion-Metastasis-Cascade Systemic Biomarkering and Targeted Drugging of Mutant BRAF-Dependent Human Cutaneous Melanomagenesis

Giannopoulou

Velentzas

Anagnostopoulos

et al. 2021

Cancers

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Melanoma is classified among the most notoriously aggressive human cancers. Despite the recent progress, due to its propensity for metastasis and resistance to therapy, novel biomarkers and oncogenic molecular drivers need to be promptly identified for metastatic melanoma. Hence, by employing nano liquid chromatography-tandem mass spectrometry deep proteomics technology, advanced bioinformatics algorithms, immunofluorescence, western blotting, wound healing protocols, molecular modeling programs, and MTT assays, we comparatively examined the respective proteomic contents of WM115 primary (n = 3955 proteins) and WM266-4 metastatic (n = 6681 proteins) melanoma cells. It proved that WM115 and WM266-4 cells have engaged hybrid epithelial-to-mesenchymal transition/mesenchymal-to-epithelial transition states, with TGF-β controlling their motility in vitro. They are characterized by different signatures of SOX-dependent neural crest-like stemness and distinct architectures of the cytoskeleton network. Multiple signaling pathways have already been activated from the primary melanoma stage, whereas HIF1α, the major hypoxia-inducible factor, can be exclusively observed in metastatic melanoma cells. Invasion-metastasis cascade-specific sub-routines of activated Caspase-3-triggered apoptosis and LC3B-II-dependent constitutive autophagy were also unveiled. Importantly, WM115 and WM266-4 cells exhibited diverse drug response profiles, with epirubicin holding considerable promise as a beneficial drug for metastatic melanoma clinical management. It is the proteome navigation that enables systemic biomarkering and targeted drugging to open new therapeutic windows for advanced disease.

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