From DNA Photolesions to Mutations, Skin Cancer and Cell Death

2005 ◽  
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Dna Photolesions

Selective cytotoxicity mechanisms and biodistribution of diamond nanoparticles on the skin cancer in C57 mouse

2021 ◽  
Author(s):  
Elham Moradi ◽  
Parvaneh Naserzadeh ◽  
Peiman Brouki Millan ◽  
Behnaz Ashtari
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Cytochrome C ◽  
Biological Activities ◽  
Cytochrome C Release ◽  
Diamond Nanoparticles ◽  
Test Conditions ◽  
Mda Content ◽  
Cell Death Signaling ◽  
High Cytotoxicity

Abstract The cytotoxicity of diamond nanoparticles (DNs) to various cell lines has been on focus by numerous scientists. The cellular toxicity system of DNs has not been fully understood or explained in skin cancer, at this point. This research was carried out to discover and reveal the potential impacts of DNs on the secluded brain, heart, liver, kidney, and skin in addition to evaluation of their cytotoxicity mechanism under test conditions. Their biological activities, for example cell viability, the level of reactive oxygen species (ROS), lipid peroxidation, cytochrome c release and Apoptosis/Necrosis were evaluated. Additionally, the bio-distribution of these nanomaterials in tissues was examined in the C57 mouse. Relying on the findings of the investigation, DNs were found to increase the ROS level, MDA content, release of cytochrome c, and cell death in skin significantly compared to other groups. In the C57 mouse, DNs were observed to have accumulated in skin tissue more intensively than they did in other organs. The present study presents for the the proof that DNs can completely induce cell death signaling in skin cancer without bringing about a high cytotoxicity in other tissues. Results suggest that DNs can be valuable in recognition of skin cancer.

scholarly journals Lunasin: A Novel Cancer Preventive Seed Peptide that Modifies Chromatin

2008 ◽  
Vol 91 (4) ◽  
pp. 932-935 ◽  
Author(s):  
Ben O de Lumen
Keyword(s):  
Growth Rate ◽  
Cell Death ◽  
Cell Division ◽  
Skin Cancer ◽  
Mammalian Cells ◽  
Constitutive Expression ◽  
Epigenetic Mechanism ◽  
Transformed Cells ◽  
Chemical Carcinogens ◽  
Core Histones

Abstract Lunasin is a novel cancer preventive peptide whose efficacy against chemical carcinogens and oncogenes has been demonstrated in mammalian cells and a skin cancer mouse model. In contrast, constitutive expression of the lunasin gene in mammalian cells leads to arrest of cell division and cell death. Isolated and characterized in soy, lunasin peptide is also documented in barley and wheat and is predicted to be present in many more seeds because of its possible role in seed development. Initial studies show that lunasin is bioavailable in mice when orally ingested. Lunasin internalizes into mammalian cells within minutes of exogenous application, and localizes in the nucleus after 18 h. It inhibits acetylation of core histones in mammalian cells but does not affect the growth rate of normal and established cancer cell lines. An epigenetic mechanism of action is proposed whereby lunasin selectively kills cells being transformed or newly transformed cells by binding to deacetylated core histones exposed by the transformation event, disrupting the dynamics of histone acetylationdeacetylation.

CDC25B and CDC25C overexpression in nonmelanoma skin cancer suppresses cell death

2019 ◽  
Vol 58 (9) ◽  
pp. 1691-1700 ◽  
Author(s):  
Jenan Al‐Matouq ◽  
Thomas R. Holmes ◽  
Laura A. Hansen
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Nonmelanoma Skin Cancer

Transgenic human programmed cell death 5 expression in mice suppresses skin cancer development by enhancing apoptosis

Life Sciences ◽  
2013 ◽  
Vol 92 (24-26) ◽  
pp. 1208-1214 ◽  
Author(s):  
Yanhui Li ◽  
Gang Zhou ◽  
Lijun La ◽  
Xiaochun Chi ◽  
Ye Cao ◽  
...  
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Programmed Cell Death ◽  
Cancer Development ◽  
Programmed Cell Death 5

scholarly journals Cyclosporine A suppresses keratinocyte cell death through MPTP inhibition in a model for skin cancer in organ transplant recipients

Mitochondrion ◽  
2010 ◽  
Vol 10 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Kimberly G. Norman ◽  
Jeffrey A. Canter ◽  
Mingjian Shi ◽  
Ginger L. Milne ◽  
Jason D. Morrow ◽  
...  
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Cyclosporine A ◽  
Organ Transplant ◽  
Transplant Recipients ◽  
Organ Transplant Recipients ◽  
Keratinocyte Cell

Anti‐programmed cell death‐1 therapy in nonmelanoma skin cancer

2016 ◽  
Vol 176 (2) ◽  
pp. 498-502 ◽  
Author(s):  
J.K. Winkler ◽  
R. Schneiderbauer ◽  
C. Bender ◽  
O. Sedlaczek ◽  
S. Fröhling ◽  
...  
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Programmed Cell Death ◽  
Nonmelanoma Skin Cancer ◽  
Programmed Cell Death 1

Biosynthesized Vitis vinifera seed gold nanoparticles induce apoptotic cell death in A431 skin cancer cells

RSC Advances ◽  
2016 ◽  
Vol 6 (85) ◽  
pp. 82205-82218 ◽  
Author(s):  
J. Grace Nirmala ◽  
S. Akila ◽  
M. S. A. Muthukumar Nadar ◽  
R. T. Narendhirakannan ◽  
Suvro Chatterjee
Keyword(s):  
Gold Nanoparticles ◽  
Cell Death ◽  
Skin Cancer ◽  
Vitis Vinifera ◽  
Cancer Cells ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
A431 Cell ◽  
Apoptotic Effects

Cytotoxic and apoptotic effects of Vitis vinifera seed gold nanoparticles on A431 cell lines.

scholarly journals Targeting 14-3-3ε activates apoptotic signaling to prevent cutaneous squamous cell carcinoma

2020 ◽  
Author(s):  
Thomas R Holmes ◽  
Jenan Al Matouq ◽  
Matti Holmes ◽  
Natasha Sioda ◽  
Justin C Rudd ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
Skin Cancer ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumor Development ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Malignant Progression ◽  
Skin Tumor ◽  
Premalignant Lesions

Abstract More than a million cases of cutaneous squamous cell carcinoma are diagnosed in the USA each year, and its incidence is increasing. Most of these malignancies arise from premalignant lesions, providing an opportunity for intervention before malignant progression. We previously documented how cytoplasmic mislocalization of CDC25A in premalignant and malignant skin cancers confers resistance to apoptotic cell death via a mechanism that depends on its interaction with 14-3-3ε. From these data, we hypothesized that 14-3-3ε overexpression drives skin tumor development and progression, such that targeting 14-3-3ε may be a useful strategy for skin cancer treatment. Like CDC25A, 14-3-3ε was overexpressed and mislocalized to the cytoplasm of both benign and malignant human skin cancer. Skin-targeted deletion of the 14-3-3ε gene reduced skin tumor development by 75% and blocked malignant progression. 14-3-3ε suppressed apoptosis through activation of Akt, leading to inhibition of BCL2 associated agonist of cell death and upregulation of Survivin. Using virtual tetrapeptide libraries, we developed a novel peptide that specifically blocked 14-3-3ε heterodimerization and thereby prevented its interaction with CDC25A. The peptide reduced prosurvival signaling, killed skin cancer cells and reduced skin tumor growth in xenograft. Normal skin keratinocytes were unaffected by inhibition or deletion of 14-3-3ε. Thus, targeting of 14-3-3ε dimerization is a promising strategy for the treatment of premalignant skin lesions.

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