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Multi-omics Sequencing reveals Epigenetic Regulation in Actinic Keratosis and Cutaneous Squamous Cell Carcinoma [850K DNA methylation array]

ABSTRACT: Cutaneous squamous cell carcinoma (cSCC) is an important type of skin cancer. It is difficult to diagnose and treat, which seriously endanger people’s the physical and mental health. Actinic keratosis (AK) induced by ultraviolet radiation is the precancerous lesion of cSCC. The mechanism of occurrence and development of cSCC is still unclear, and the research on epigenetics is even less. In this project, we intend to study the mechanism of cSCC, especially the transformation from normal skin to AK, cSCC and the metastasis in late stage of cSCC, using multi-omics sequencing technology with experimental methods. Through the integrated analysis of multi-omics information such as DNA methylation, RNA methylation, chromatin accessibility and transcriptome, we obtained the epigenetic map of different stages of cSCC and identified the potential key epigenetic driving factors for cSCC. This project provided an important scientific basis for the clinical treatment and drug development of cSCC, as well as method reference for the study of other cancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE277273 | GEO | 2025/12/04

REPOSITORIES: GEO

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Multi-omics Sequencing reveals Epigenetic Regulation in Actinic Keratosis and Cutaneous Squamous Cell Carcinoma [ATAC-seq]

Project description:Cutaneous squamous cell carcinoma (cSCC) is an important type of skin cancer. It is difficult to diagnose and treat, which seriously endanger people’s the physical and mental health. Actinic keratosis (AK) induced by ultraviolet radiation is the precancerous lesion of cSCC. The mechanism of occurrence and development of cSCC is still unclear, and the research on epigenetics is even less. In this project, we intend to study the mechanism of cSCC, especially the transformation from normal skin to AK, cSCC and the metastasis in late stage of cSCC, using multi-omics sequencing technology with experimental methods. Through the integrated analysis of multi-omics information such as DNA methylation, RNA methylation, chromatin accessibility and transcriptome, we obtained the epigenetic map of different stages of cSCC and identified the potential key epigenetic driving factors for cSCC. This project provided an important scientific basis for the clinical treatment and drug development of cSCC, as well as method reference for the study of other cancers.

2025-12-04 | GSE277274 | GEO

Multi-omics Sequencing reveals Epigenetic Regulation in Actinic Keratosis and Cutaneous Squamous Cell Carcinoma [m6A-seq]

2025-12-04 | GSE277275 | GEO

Single cell transcriptomes of genetic landscape from actinic keratosis to cutaneous squamous cell carcinoma

Project description:Here, we performed scRNA-seq to compare the transcriptomes of individual cells from three groups: (1) healthy sun-exposed skin; (2) AK samples; (3) cSCC samples. A total of 81792 cells from 8 AK samples, 3 cSCC samples and 3 control skin tissue were characterized, which comprising representatives from each of the major dermal cell types. Our results demonstrate the heterogeneity within tissues/patients and corroborated the effect of the tumor environment during carcinogenesis, especially immune cell populations. Additionally, we identified a list of gene expression changes that affected several known cancerous pathways, with potential evolution trajectory from a subset of AK premalignant cells to cSCC cells. Our findings will improve current understanding about the mechanism of AK-cSCC progression, and are potentially valuable in providing novel precautionary/ therapeutic markers.

2025-10-28 | GSE200334 | GEO

Single-cell Sequencing Highlights Heterogeneity and Malignant Progression in Actinic Keratosis and Cutaneous Squamous Cell Carcinoma

Project description:Cutaneous squamous cell carcinoma (cSCC) is the second most frequent of the keratinocyte-derived malignancies with actinic keratosis (AK) as a precancerous lesion. To comprehensively delineate the underlying mechanisms for the whole progression from normal skin to AK to invasive cSCC, we performed single-cell RNA-seq (scRNA-seq) to acquire the transcriptomes of 138,982 cells from 13 samples of six patients including AK, squamous cell carcinoma in situ (SCCIS), cSCC and their normal tissues, covering comprehensive clinical courses of cSCC. We identified diverse cell types, including important subtypes with different gene expression profiles and functions in major keratinocytes. In SCCIS, we discovered the malignant subtypes of basal cells with differential proliferative and migration potential. Differentially expressed genes (DEG) analysis screened out multiple key driver genes including transcription factors (TFs) along AK to cSCC progression. Immunohistochemistry (IHC) / immunofluorescence (IF) experiments and single-cell ATAC sequencing (scATAC-seq) data verified the expression changes of these genes. The functional experiments confirmed the important roles of these genes in regulating cell proliferation, apoptosis, migration and invasion in cSCC tumor. Furthermore, we comprehensively described the tumor microenvironment (TME) landscape and potential keratinocyte-TME crosstalk in cSCC providing theoretical basis for immunotherapy. Together, our findings provide a valuable resource for deciphering the progression from AK to cSCC and identifying potential targets for anticancer treatment of cSCC.

2023-01-12 | GSE193304 | GEO

Key differences identified between actinic keratosis and cutaneous squamous cell carcinoma by transcriptome profiling

Project description:Cutaneous squamous cell carcinoma (cSCC) is one of the most common malignancies in fair skinned populations worldwide and its incidence is increasing. Despite previous observations of multiple genetic abnormalities in cSCC, the oncogenic process remains elusive. The purpose of this study was to investigate the transcriptomes of cSCC and actinic keratoses (AK), to elucidate key differences between precursor AK lesions and invasive carcinoma. This study identified 196 genes that are differentially expressed between AK and cSCC, with enrichment for processes including epidermal differentiation, cell migration, cell cycle regulation and metabolism. Gene set enrichment analysis highlighted a key role for the MAPK pathway in the transition from AK to cSCC. Furthermore, the differentiation status of the tumor influenced the gene expression profile, which may have implications for drug sensitivity and response in clinical trials. These data indicate that progression to cSCC is associated with a complex pattern of molecular changes. We have identified relevant pathways involved in this process, in particular that the MAPK pathway may be pivotal to the transition from AK and may represent a potential therapeutic target. RNA was extracted by laser capture microdissection from 10 AK and 30 cSCC, for analysis using the Affymetrix HG U133 Plus 2.0 microarrays. The cSCC samples included a range of histological diagnoses (well differentiated through to poorly differentiatied) from both immunocompetent and immunosuppressed patients.

2014-01-21 | E-GEOD-45216 | biostudies-arrayexpress

Key differences identified between actinic keratosis and cutaneous squamous cell carcinoma by transcriptome profiling

2014-01-21 | GSE45216 | GEO

Differential proteomic analysis of actinic keratosis, Bowen's disease and cutaneous squamous cell carcinoma by label-free LC-MS/MS

Project description:BACKGROUND: The boundaries between actinic keratosis (AK), Bowen's disease (BD), and cutaneous squamous cell carcinoma (cSCC) are sometimes not clear. Large-scale proteomic profiling studies of these lesions are also non-existent. OBJECTIVE: To evaluate proteomic changes between normal epidermis, AK, BD and cSCC that could support a molecular classification and improve our understanding of disease progression. METHODS: Microdissected formalin-fixed paraffin embedded samples of normal epidermis (n = 4, pooled), AK (n = 10), BD (n = 10) and cSCC (n = 10) were analyzed by mass spectrometry. Following normalization and multiple testing adjustments, differential abundance analysis was performed using Linear Models for Microarray data. Proteins were filtered for significance (adjusted p-value ≤ 0.05) and fold change of at least ±1.5. Comparative bioinformatics analysis was performed using Ingenuity Pathway Analysis (IPA) software. Proteomic findings were subsequently substantiated using immunohistochemistry. RESULTS: 2073 unique proteins were identified. cSCC had the highest number of differentially abundant proteins (63 proteins) followed by BD (58 proteins) and AK (46 proteins). Six proteins (APOA1, ALB, SERPINA1, HLA-B, HP and TXNDC5) were differentially abundant in cSCC compared to AK. Immunohistochemical analysis corroborated changes in MIF, RPL37A and TXNDC5. IPA analysis predicted that cell proliferation, angiogenesis and inflammatory reactions were significantly activated in cSCC compared to BD and AK. Cell death and DNA damage were predicted to be inhibited in BD. CONCLUSION: Our study supports the concept that AK and BD are precursors of cSCC. The identification of proteome changes indicates disruption of repair, pro-apoptotic, and tumor promoting pathways. Our findings will help select targets for classification and treatment.

2018-11-21 | PXD011609 | Pride

Primary Keratinocyte Model of Actinic Keratosis Reveals UV-Induced DNA Damage Accumulation and Persistent Interferon Signaling

Project description:Actinic keratosis (AK) is a precancerous, UV-induced skin lesion that can progress to cutaneous squamous cell carcinoma (cSCC). While UV radiation is known to drive mutations and immunosuppression in the skin, keratinocyte-intrinsic responses to chronic, low-dose solar UV exposure have been insufficiently studied in AK. We established a patient-derived in vitro model using primary keratinocytes from AK lesions and age-matched, sun-exposed skin to investigate how repeated low-dose UV irradiation shapes keratinocyte stress responses. Integrating high-content morphological profiling, cyclobutane pyrimidine dimer (CPD) quantification and bulk RNA sequencing, we observed pronounced morphological remodeling and persistent DNA damage in AK keratinocytes despite activation of DNA repair and unfolded protein response pathways. Transcriptomic analyses revealed constitutive and UV-enhanced interferon signaling in AK cells, including upregulation of innate DNA sensing and ISGylation genes. Meta-analysis of five independent datasets confirmed interferon pathway activation as a conserved feature of AK, and IFN-α exposure further sensitized AK keratinocytes to UV-induced CPD formation. Our primary model thus uncovers sustained interferon signaling and attenuated DNA damage repair as key keratinocyte-intrinsic features of AK, suggesting that chronic interferon responses may modulate UV-induced damage and contribute to early photocarcinogenic processes.

2025-12-03 | GSE305980 | GEO

THE GENOMIC LANDSCAPE OF ACTINIC KERATOSIS

Project description:Actinic keratoses (AK) are lesions of epidermal keratinocyte dysplasia and are pre-cursor lesions to invasive cutaneous squamous cell carcinoma (cSCC). Identifying the specific genomic alterations driving the progression of normal skin to AK and invasive cSCC is challenging due to the massive, ultraviolet radiation-induced mutational burden characteristic to these lesions. Here, we present the largest whole exome sequencing study to date on AK with matched cSCC and demonstrate that AK and cSCC are almost indistinguishable at the genomic level, in terms of mutational burden, patterns of driver gene mutations and copy number alterations. We identified 44 significantly mutated AK driver genes through our established bioinformatics pipeline and demonstrate these genes are similarly mutated in cSCC. We also identified mutational signature-32 exclusively in AK from patients exposed to azathioprine, providing further, compelling evidence for this drugÃ¢Â€Â™s role in keratinocyte carcinogenesis, likely through its blocking of transcription coupled repair. We demonstrated that cSCC had higher levels of intra-sample heterogeneity than AK and that several signaling pathways, including immune-related signaling and TGF-beta signaling were significantly more mutated in cSCC. Integrating our findings with independent gene expression data confirms that dysregulated TGF-beta signaling may represent the critical pathway in the progression from AK to cSCC.

| EGAS00001004243 | EGA

Ingenol mebutate induces profound inflammatory and wound healing responses in uninvolved and actinic keratosis skin

Project description:We studied the transcriptomic profile of actinic keratosis (AK) skin compared to matched samples from uninvolved skin (US) before and after treatment with ingenol mebutate gel. We found that AK has a distinct mRNA profile that separates it from uninvolved skin. In particular, numerous genes associated with epidermal development and keratinocyte differentiation, such as LCE3D, SPRR1A, PI3 and several genes in the keratin family were highly expressed in AK0 skin, but not in US0, in line with the hyperkeratosis characteristic for AK. Topical application of ingenol mebutate had a profound effect on the gene expression profile, and interestingly, many more genes were affected in US than in AK. Enrichment analysis revealed that the main responses to ingenol mebutate treatment of both US and AK were inflammatory response, response to wounding, and wound healing. 30 skin biopsies were analysed; 5 from each of 6 AK patients. Before initiation of treatment, baseline biopsies were taken from one AK lesion (AK0) and from uninvolved skin (US0). A third biopsy was taken after day 1 application of ingenol mebutate from one AK lesion (AK1). The fourth and fifth biopsies were obtained one day after the second topical application with ingenol mebutate from an AK lesion (AK2) and from uninvolved skin (US2), respectively.

2016-03-31 | E-GEOD-63107 | biostudies-arrayexpress

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