Generation and characterization of CRISPR-Cas9-mediated XPC gene knockout in human skin cells

Xeroderma pigmentosum group C (XPC) is a versatile protein crucial for sensing DNA damage in the global genome nucleotide excision repair (GG-NER) pathway. This pathway is vital for mammalian cells, acting as their essential approach for repairing DNA lesions stemming from interactions with environmental factors, such as exposure to ultraviolet (UV) radiation from the sun. Loss-of-function mutations in the XPC gene confer a photosensitive phenotype in XP-C patients, resulting in the accumulation of unrepaired UV-induced DNA damage. This remarkable increase in DNA damage tends to elevate by 10,000-fold the risk of developing melanoma and non-melanoma skin cancers. To date, creating accurate and reproducible models to study human XP-C disease has been an important challenge. To tackle this, we used CRISPR-Cas9 technology in order to knockout the XPC gene in various human skin cells (keratinocytes, fibroblasts, and melanocytes). After validation of the knockout in these edited skin cells, we showed that they recapitulate the major phenotypes of XPC mutations: photosensitivity and the impairment of UV-induced DNA damage repair. Moreover, these knockout cells demonstrated a reduced proliferative capacity compared to their respective controls. Finally, to better mimic the disease environment, we built a 3D reconstructed skin using these XPC knockout skin cells. This model exhibited an abnormal behavior, showing an extensive remodeling of its extracellular matrix compared to normal skin. Analyzing the composition of the fibroblast secretome revealed a significant augmented shift in the inflammatory response following XPC knockout. Our innovative "disease on a dish" approach can provide valuable insights into the molecular mechanisms underlying XP-C disease, paving the way to design novel preventive and therapeutic strategies to alleviate the disease phenotype. Also, given the high risk of skin cancer onset in XP-C disease, our new approach can serve as a link to draw novel insights into this elusive field.

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Publication Details

Journal
Scientific Reports
Published
2024-12-28
DOI
https://doi.org/10.1038/s41598-024-81675-6
Citations
5
Primary Topic
CRISPR and Genetic Engineering
Type
article
Field-Weighted Citation Impact
1.17

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article

Generation and characterization of CRISPR-Cas9-mediated XPC gene knockout in human skin cells

Jos P.H. Smits, Ali Nasrallah, Eric Sulpice, Jérôme Rambert et al.
5 citations
Scientific Reports
CRISPR and Genetic Engineering
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article

Generation and characterization of CRISPR-Cas9-mediated XPC gene knockout in human skin cells

Jos P.H. Smits, Ali Nasrallah, Eric Sulpice, Jérôme Rambert, Hamid Rezvani, Farah Kobaisi, Walid Rachidi, Ahmad Hammoud
article en
5 citations

Abstract

Xeroderma pigmentosum group C (XPC) is a versatile protein crucial for sensing DNA damage in the global genome nucleotide excision repair (GG-NER) pathway. This pathway is vital for mammalian cells, acting as their essential approach for repairing DNA lesions stemming from interactions with environmental factors, such as exposure to ultraviolet (UV) radiation from the sun. Loss-of-function mutations in the XPC gene confer a photosensitive phenotype in XP-C patients, resulting in the accumulation of unrepaired UV-induced DNA damage. This remarkable increase in DNA damage tends to elevate by 10,000-fold the risk of developing melanoma and non-melanoma skin cancers. To date, creating accurate and reproducible models to study human XP-C disease has been an important challenge. To tackle this, we used CRISPR-Cas9 technology in order to knockout the XPC gene in various human skin cells (keratinocytes, fibroblasts, and melanocytes). After validation of the knockout in these edited skin cells, we showed that they recapitulate the major phenotypes of XPC mutations: photosensitivity and the impairment of UV-induced DNA damage repair. Moreover, these knockout cells demonstrated a reduced proliferative capacity compared to their respective controls. Finally, to better mimic the disease environment, we built a 3D reconstructed skin using these XPC knockout skin cells. This model exhibited an abnormal behavior, showing an extensive remodeling of its extracellular matrix compared to normal skin. Analyzing the composition of the fibroblast secretome revealed a significant augmented shift in the inflammatory response following XPC knockout. Our innovative "disease on a dish" approach can provide valuable insights into the molecular mechanisms underlying XP-C disease, paving the way to design novel preventive and therapeutic strategies to alleviate the disease phenotype. Also, given the high risk of skin cancer onset in XP-C disease, our new approach can serve as a link to draw novel insights into this elusive field.

Scientific ReportsVol. 14(1)
Radboud University Nijmegen (NL), Université de Bordeaux (FR), Inserm (FR), Commissariat à l'Énergie Atomique et aux Énergies Alternatives (FR), Radboud University Medical Center (NL), CEA Grenoble (FR), Bordeaux Population Health (FR), Radboud Institute for Molecular Life Sciences (NL), BoRdeaux Institute of onCology (FR), Université Grenoble Alpes (FR)
Agence Nationale de la Recherche
Openalex Percentile: Top 21%
CRISPR and Genetic Engineering
1.17
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