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P63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235467 | GEO | 2026/08/28

REPOSITORIES: GEO

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p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [ChIP-Seq]

Project description:Aberrant expression of transcriptional regulators can affect oncogenic gene expression programs in cancer. Mutations in the tumor suppressor p53 are commonly found in UV-damaged skin and protect damaged epidermal cells from senescence and or oncogene-induced apoptosis, favoring cancer formation. In contrast, the other p53 family members p63 and p73 are rarely mutated in cancer and p63 is often amplified or overexpressed in lung, esophagus, and head and neck squamous cell carcinoma (SCC). Here, we demonstrate that both p63 and p73 are required for cell proliferation in epidermal cells and in skin SCC and are overexpressed in preneoplastic lesions and in skin SCCs. p63/p73 form heterotetramers and co-occupy thousands of regulatory regions, jointly controlling a transcriptional program that promotes cell proliferation and tumorigenesis. The combination of gene knockdown with transcriptomic and epigenetic analyses revealed that p63 and p73 control a transcriptional feed-forward circuit that sustains cell proliferation. We find that in skin SCC a key signaling pathway downstream of p63/p73 is the Epidermal Growth Factor Receptor (EGFR)/MAP kinase. p63/p73 directly and positively control transcription of the EGFR ligands, among which amphiregulin (AREG) is the most highly expressed in skin SCC. Like p63/p73, AREG is critical to maintain skin SCC proliferative potential, anchorage independent growth, and to promote tumorigenesis. Thus, p63 and p73 act as oncogenic drivers in skin SCC, with AREG being a crucial non-cell-autonomous effector downstream of p63 and p73 in skin SCC formation.

2026-08-28 | GSE235461 | GEO

p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [RNA-Seq]

2026-08-28 | GSE235459 | GEO

p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs

Project description:p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs

| PRJNA986102 | ENA

p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [RNA-Seq]

Project description:p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [RNA-Seq]

| PRJNA986095 | ENA

p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [ChIP-Seq]

Project description:p63 and p73 cooperate to promote cutaneous squamous cell carcinoma through largely overlapping transcriptional programs [ChIP-Seq]

| PRJNA986110 | ENA

p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma.

Project description: Not available

| S-EPMC12280952 | biostudies-literature

DARPins detect the formation of hetero-tetramers of p63 and p73 in epithelial tissues and in squamous cell carcinoma.

Project description: Not available

| S-EPMC10570377 | biostudies-literature

Structural diversity of p63 and p73 isoforms.

Project description: Not available

| S-EPMC9091270 | biostudies-literature

p63 and ZNF148 cooperate to regulate head and neck squamous cell carcinoma

Project description:Head and neck squamous cell carcinoma (HNSCC) is a common and aggressive malignancy. While significant advances have been made in the management of low-grade cancer, treatment of advanced HNSCC remains challenging. Here, we used a proteomic approach to discover novel binding partners of the oncogene p63, the most frequently amplified transcription factor in HNSCC. We identified a zinc finger protein, ZNF148, which is coexpressed and physically binds p63 in carcinoma cells. Genome occupancy analyses identified a functional transcribed enhancer-derived RNA (eRNA) upstream of the CCND1 gene occupied by both factors. Mechanistically, p63 and ZNF148 control transcription of this eRNA, leading to overexpression of cyclin D1 to reinforce tumour cell proliferation. Importantly, this axis is specific for cancer cells and remains inactive in normal epithelial cells. The expression levels of these factors and the eRNA are positively correlated in cancer and associated with advanced stage and metastasis. Collectively, our data reveal a novel molecular pathway controlling HNSCC progression and identifies potential selective targets for cancer treatment.

2025-06-18 | GSE279161 | GEO

Epigenetic regulation of iASPP-p63 feedback loop in cutaneous squamous cell carcinoma

Project description:Keratinocyte skin cancer, comprising cutaneous squamous (cSCC) and basal cell carcinoma, is the most common malignancy in the UK. P53 is frequently mutated in cSCC. iASPP is a key inhibitor of p53 and NF-kB signalling pathways and has been documented as highly expressed in several types of human cancer. We have previously identified an autoregulatory feedback loop between iASPP and p63, which is critical in epidermal homeostasis. We hypothesised a potential role for dysregulation of this axis in the pathogenesis of keratinocyte malignancies. Immunostaining of 116 cSCC clinical samples revealed increased iASPP and ΔNp63 expression but also highlighted a significant alteration of iASPP cellular localisation, with consequent deregulation of its function. Expression patterns, functionality, gene and microRNA expression analysis were further investigated in 10 cSCC cell lines. Our data suggest that whilst direct effects of iASPP and p63 upon each other’s expression are maintained in cSCC, epigenetic dysregulation of the feedback loop occurs at the microRNA level by a novel mechanism controlling p63 expression. We demonstrate that this autoregulatory feedback loop controls cell migration in cSCC by blocking EMT and promoting proliferation, and provides future directions for clinical biomarker and therapeutic target discovery in cutaneous SCC.

2019-11-20 | GSE123189 | GEO

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