Effect of Infliximab on the UVB-Induced Apoptosis of Keratinocytes Infected by HPV38 E6/E7

Aubin, F.; Gheit, Tarik; Prétet, Jean‐Luc; Tommasino, Massimo; Mougin, Christiane

doi:10.1155/2013/907189

Cited by 1 publication

(1 citation statement)

References 13 publications

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“…A day after the passage, cells received fresh growth medium supplemented with/without TNFα (10 ng/mL; Sigma-Aldrich, Munich, Germany) or TNFα and infliximab (IFX) (200 μg/ mL; Centocor Biotech Inc., County Cork, Ireland). Dose of infliximab was determined in pilot experiments based on the dose range of already published data [20,21]. The stimulation time with TNFα alone or TNFα/IFX was 24 h. Then, cells were further treated for 18 h with soluble, human, recombinant TRAIL (KillerTRAIL, Alexis, Gruenberg, Germany ALX-201-073-C020; 30 ng/mL or 30, 15, 7.5 ng/mL for dose-dependent experiment), or for 48 h with 5FU (40 μmol; Sigma-Aldrich, Munich, Germany).…”

Section: Cell Lines and Cell Culture Conditionsmentioning

confidence: 99%

Ambivalent Effects of Tumor Necrosis Factor Alpha on Apoptosis of Malignant and Normal Human Keratinocytes

Kokolakis

Sabat

Krüger‐Krasagakis

et al. 2021

Skin Pharmacol Physiol

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Introduction: Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that may paradoxically induce either apoptosis or cell survival. It mediates its activity through binding of TNF-receptor (TNFR) 1 or 2. TNFR1 is mainly responsible for transmitting apoptotic signals. The activation of apoptotic mechanisms can either be intrinsic (mitochondrial) or extrinsic (death receptors). Death ligands such as TNF-related apoptosis-inducing ligand (TRAIL) specifically induce extrinsic apoptosis, while cytostatic drugs such as 5-fluorouracil (5FU) induce intrinsic apoptosis. Objectives: To investigate the effects of TNFα on apoptosis in malignant and normal human keratinocytes. Methods: Human cutaneous squamous cell carcinoma (SCC) cell line SCC-13 and immortalized human keratinocytes HaCaT as well as primary normal human keratinocytes (PNHK) were stimulated with TNFα and then treated either with TRAIL or 5FU. Cell viability and cell proliferation, DNA fragmentation, apoptosis, and cytotoxicity were determined by WST-1 proliferation assay, ELISA, flow cytometry, and colorimetric analysis of lactate dehydrogenase, respectively. In addition, Western blotting was performed for analysis of caspase-3. Results: TNFα affected viability of SCC-13 and HaCaT cells in combination with 5FU or TRAIL. In contrast, TNFα did not influence cell viability of PNHK. It enhanced the apoptotic effects of both extrinsic and intrinsic stimuli in SCC-13 and HaCaT. In clear contrast, TNFα protected PNHK against TRAIL- and 5FU-induced apoptosis. The effects were dose-dependent and TNFα-specific; furthermore, the apoptosis pathway was caspase-dependent. Conclusions: In summary, opposing effects of TNFα in malignant versus normal human keratinocytes were observed with possibly relevant clinical implications, when patients are treated with TNFα inhibitors.

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Section: Cell Lines and Cell Culture Conditionsmentioning

confidence: 99%