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P63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

ABSTRACT: Analysis of P63-regulated genes at gene expression level. The hypothesis tested in the present study was that P63 regulates specific epithelial-to-mesenchymal transition states in breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128190 | GEO | 2019/03/13

REPOSITORIES: GEO

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p63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

Project description:p63 regulated epithelial-to-mesenchymal transition state heterogeneity drives collective invasion.

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ΔNp63-Regulated Epithelial-to-Mesenchymal Transition State Heterogeneity Confers a Leader-Follower Relationship That Drives Collective Invasion.

Project description:Defining how interactions between tumor subpopulations contribute to invasion is essential for understanding how tumors metastasize. Here, we find that the heterogeneous expression of the transcription factor ΔNp63 confers distinct proliferative and invasive epithelial-to-mesenchymal transition (EMT) states in subpopulations that establish a leader-follower relationship to collectively invade. A ΔNp63-high EMT program coupled the ability to proliferate with an IL1α- and miR-205-dependent suppression of cellular protrusions that are required to initiate collective invasion. An alternative ΔNp63-low EMT program conferred cells with the ability to initiate and lead collective invasion. However, this ΔNp63-low EMT state triggered a collateral loss of fitness. Importantly, rare growth-suppressed ΔNp63-low EMT cells influenced tumor progression by leading the invasion of proliferative ΔNp63-high EMT cells in heterogeneous primary tumors. Thus, heterogeneous activation of distinct EMT programs promotes a mode of collective invasion that overcomes cell intrinsic phenotypic deficiencies to induce the dissemination of proliferative tumor cells. SIGNIFICANCE: These findings reveal how an interaction between cells in different EMT states confers properties that are not induced by either EMT program alone.

| S-EPMC8406430 | biostudies-literature

Genetic heterogeneity within collective invasion packs drives leader and follower cell phenotypes.

Project description:Collective invasion, the coordinated movement of cohesive packs of cells, has become recognized as a major mode of metastasis for solid tumors. These packs are phenotypically heterogeneous and include specialized cells that lead the invasive pack and others that follow behind. To better understand how these unique cell types cooperate to facilitate collective invasion, we analyzed transcriptomic sequence variation between leader and follower populations isolated from the H1299 non-small cell lung cancer cell line using an image-guided selection technique. We now identify 14 expressed mutations that are selectively enriched in leader or follower cells, suggesting a novel link between genomic and phenotypic heterogeneity within a collectively invading tumor cell population. Functional characterization of two phenotype-specific candidate mutations showed that ARP3 enhances collective invasion by promoting the leader cell phenotype and that wild-type KDM5B suppresses chain-like cooperative behavior. These results demonstrate an important role for distinct genetic variants in establishing leader and follower phenotypes and highlight the necessity of maintaining a capacity for phenotypic plasticity during collective cancer invasion.

| S-EPMC6803364 | biostudies-literature

Transcription profiling of skin from p63 null and wild type mice to identify genes that are directly or indirectly regulated by p63.

Project description:In the absence of p63 expression, the epidermis fails to commit to stratification, resulting in aborted skin development. In this study, gene expression profiles of E18.5 p63 null and wt skin, were compared in an effort to identify genes that are directly or indirectly regulated by p63. Experiment Overall Design: E18.5 embryos were obtained from matings between p63 heterozygous mice. RNA was isolated from the skin of two p63 null and two wild type embryos.

2007-09-07 | E-GEOD-3108 | biostudies-arrayexpress

p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ChIP-Seq]

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ATAC-Seq]

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siRNA profiling of human keratinocyte and squamous cell carcinoma cell lines knocked down with p63 reveals loss of p63 leads to increased cell migration and up-regulation of genes involved in invasion and metastasis

Project description:p63, a homologue of the tumor suppressor p53, is critical for the development and maintenance of squamous epithelia. p63 is specifically expressed in the basal layers of stratified epithelial tissues and is considered a specific marker for cells of this type. The role of p63 in tumorigenesis remains poorly defined. Numerous studies have highlighted the oncogenic potential of the predominant p63 isoform DeltaNp63alpha; however, data suggest that other p63 proteins can act as tumor suppressors or alter the metastatic potential of tumors. DeltaNp63alpha can act as a transcriptional repressor, but the link between the transcriptional functions of p63 and its biological role is still unclear. In this study, we used a loss-of-function approach to investigate the transcriptional programs controlled by p63. Disruption of p63 in squamous cell lines resulted in down-regulation of transcripts specifically expressed in squamous tissues and a significant alteration of keratinocyte differentiation. Interestingly, we found that disruption of p63 led to up-regulation of markers of nonepithelial tissues (mesenchyme and neural tissue) in both primary and immortalized squamous cells. Many of these up-regulated genes are associated with increased capacity for invasion and metastasis in tumors. Furthermore, loss of p63 expression was accompanied by a shift toward mesenchymal morphology and an increase in motility in primary keratinocytes and squamous cell lines. We conclude that loss of endogenous p63 expression results in up-regulation of genes associated with invasion and metastasis, and predisposes to a loss of epithelial and acquisition of mesenchymal characteristics. These findings have implications for the role of p63 in both development and tumorigenesis.

2007-11-11 | E-GEOD-4975 | biostudies-arrayexpress

Control of breast cancer cell migration by a p63-regulated signaling network (RNA)

Project description:Through analysis of a high-content screen we discovered that mir-203 can impair cell migration by suppressing p63 expression. We further determined that p63 promotes motility by inducing the expression of multiple target genes.

2014-10-22 | GSE62568 | GEO

Control of breast cancer cell migration by a p63-regulated signaling network (miRNA)

2014-10-22 | GSE62567 | GEO

USP22 drives colorectal cancer invasion and metastasis via epithelial-mesenchymal transition by activating AP4.

Project description:Ubiquitin specific peptidase 22 (USP22), a putative cancer stem cell marker, is overexpressed in liver metastases of colorectal cancer (CRC). However, the mechanism by which USP22 promotes CRC metastasis remains largely unknown. Here, we report that USP22 and AP4 are simultaneously overexpressed during TGF-?1-induced CRC cell epithelial-mesenchymal transition (EMT). USP22 up-regulation enhances CRC cell migration and invasion and EMT-related marker and AP4 expression, but these effects are partly blocked by AP4 knockdown. In addition, USP22 binds to the promoter region of AP4 to activate its transcription. In vivo, elevated USP22 expression promotes CRC cell metastasis to the lungs in nude mice, as evidenced by the fact that CRC metastatic nodules stain deeply positive for USP22 and AP4. In human CRC tissues, the genes encoding USP22 and AP4 are overexpressed in metastatic liver lesions compared with primary cancer tissues, and their overexpression is significantly associated with poor CRC patient survival. These findings indicate that USP22 and AP4 may serve as prognostic markers for predicting the risk of developing distant metastases in CRC.

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