Expression data from sorted epithelial CD34+ expressing cells from DMBA/TPA induced skin tumors
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE31465 | GEO | 2011/09/07
SECONDARY ACCESSION(S): PRJNA145661
REPOSITORIES: GEO
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Project description:Transcriptional profile of control and VEGF overexpressing FACS-isolated CD34+ Cancer stem cells from DMBA/TPA induced skin tumours Tumours were digested in collagenase I (Sigma) for 2 hours at 37°C on a rocking plate. Collagenase I activity was blocked by addition of EDTA (5mM) and then rinced in PBS supplemented with 2%FCS. After tumour digestion, cells were first incubated in PBS complemented with 30% FCS to block Fc receptors for 15 min at room temperature. Immunostaining was performed using biotin-conjugated anti-CD34 (clone RAM34; BD Pharmingen), FITC-conjugated anti-α6-integrin (clone GoH3; BD Pharmingen), PE-conjugated anti-CD45 (clone 30F11, eBiosciences), PE-conjugated anti CD31 (clone MEC13.3; BD Pharmingen), PE-conjugated anti-CD140a (clone APA5; eBiosciences), APC-Cy7-conjugated anti-Epcam (clone G8.8; Biolegend) by incubation for 30min on ice. Cells were washed and stained using APC-conjugated Streptavidin (BD Pharmingen) for 20min on ice. Living tumour cells were selected by forward scatter, side scatter and by Hoechst dye exclusion. Fluorescence-activated cell sorting analysis was performed using FACSAria and FACSDiva software (BD Biosciences). Sorted cells were collected in the lysis buffer provided by the manufacturer (Microprep kit, RNeasy, Stratagene) and RNA extraction was performed according to the manufacturer's protocol. Total RNA was analysed using Mouse whole genome 430 2.0 array from Affymetrix at the VIB microarray facility (KU – Leuven, Belgium). We analyzed CD34+ TECs isolated by FACS from a K14CreER:Rosa-VEGF-164 and control mice. Analysis of the microarray was perfored by the VIB microarray facility (KU – Leuven, Belgium).
2011-09-06 | E-GEOD-31465 | biostudies-arrayexpress
Project description:We compared expressions of cancer-related genes (tumor suppressor genes and oncogenes) in the skin epidermis between FVB mice treated with DMBA/TPA and control animals. Bulk RNA-seq analyses revealed that in contrast to control animals, epidermis of mice treated with DMBA is characterized by upregulation of the genes enriched for immune response pathways, whereas downregulated genes were involved in the control of extracellular matrix remodeling and wound healing. In mouse epidermis treated by DMBA/TPA, transcriptional response to DMBA/TPA at the pre-tumor stage was accompanied by upregulation of the genes controlling epidermal differentiation, oncogenes including the components of Wnt signaling pathway, as well as of selected tumor suppressor genes.
2026-07-09 | GSE334587 | GEO
Project description:We compared expressions of cancer-related genes (tumor suppressor genes and oncogenes) in the skin epidermis between Naked mole-rats treated with DMBA/TPA and control animals. Bulk RNA-seq analyses revealed that in contrast to control animals, epidermis of Naked mole-rats treated with DMBA/TPA is characterized by increased expression of anti-cancer genes, activation of genes controlling ferroptosis, as well as by downregulation of numerous oncogenes including components of NF-kB, Wnt and tyrosine kinase signaling pathways.
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Project description:African spiny mice, Acomys cahirinus (Acomys), is an emerging mammalian model for regeneration studies because of its ability to morphologically and functionally regenerate several tissues. However, as limited regenerative abilities in most mammals are viewed as an antitumor strategy, it is intriguing how Acomys balance regeneration and tumor suppression. To date, no spontaneous tumors have been reported in Acomys, suggesting it may be resistant to cancer. In this study, we use in vitro and in vivo approaches to investigate if A. cahirinus is susceptible to carcinogenesis. We report that, like mice, two oncogenic hits - activation of oncogenic RasG12V and inactivation of p53 or pRb - are sufficient to transform skin fibroblasts from A. cahirinus. However, surprisingly, active p53 dramatically reduces the tumor forming ability of the transformed fibroblasts. In the DMBA/TPA treatment model of in vivo skin carcinogenesis with animals aged 1-1.5 years, C57BL/6 laboratory mice formed pre-malignant skin tumors in 22 weeks, while A. cahirinus did not show any effects. A longer TPA treatment period of 30 weeks induced benign sebaceous adenomas in A. cahirinus. This showed that A. cahirinus was resistant to squamous skin carcinogenesis typically induced by DMBA/TPA treatment. A. cahirinus showed significantly higher upregulation of immune response and differentially expressed tumor suppressors and oncogenes in DMBA/TPA-treated skin when compared to mice. Wnt/β-catenin signaling, a major mediator of squamous carcinogenesis associated with DMBA/TPA treatment, was inhibited in A. cahirinus. Several Wnt/β-catenin targets and effector transcription factors, especially Lef1, were transcriptionally downregulated in A. cahirinus. Overall, our study shows that A. cahirinus may be resistant to DMBA/TPA-induced squamous carcinogenesis, and this resistance may be mediated by a strong immune response and the inhibition of Wnt/β-catenin signaling.
2025-10-15 | GSE287008 | GEO
Project description:African spiny mice, Acomys cahirinus (Acomys), is an emerging mammalian model for regeneration studies because of its ability to morphologically and functionally regenerate several tissues. However, as limited regenerative abilities in most mammals are viewed as an antitumor strategy, it is intriguing how Acomys balance regeneration and tumor suppression. To date, no spontaneous tumors have been reported in Acomys, suggesting it may be resistant to cancer. In this study, we use in vitro and in vivo approaches to investigate if A. cahirinus is susceptible to carcinogenesis. We report that, like mice, two oncogenic hits - activation of oncogenic RasG12V and inactivation of p53 or pRb - are sufficient to transform skin fibroblasts from A. cahirinus. However, surprisingly, active p53 dramatically reduces the tumor forming ability of the transformed fibroblasts. In the DMBA/TPA treatment model of in vivo skin carcinogenesis with animals aged 1-1.5 years, C57BL/6 laboratory mice formed pre-malignant skin tumors in 22 weeks, while A. cahirinus did not show any effects. A longer TPA treatment period of 30 weeks induced benign sebaceous adenomas in A. cahirinus. This showed that A. cahirinus was resistant to squamous skin carcinogenesis typically induced by DMBA/TPA treatment. A. cahirinus showed significantly higher upregulation of immune response and differentially expressed tumor suppressors and oncogenes in DMBA/TPA-treated skin when compared to mice. Wnt/β-catenin signaling, a major mediator of squamous carcinogenesis associated with DMBA/TPA treatment, was inhibited in A. cahirinus. Several Wnt/β-catenin targets and effector transcription factors, especially Lef1, were transcriptionally downregulated in A. cahirinus. Overall, our study shows that A. cahirinus may be resistant to DMBA/TPA-induced squamous carcinogenesis, and this resistance may be mediated by a strong immune response and the inhibition of Wnt/β-catenin signaling.
2025-10-15 | GSE287009 | GEO
Project description:In this analysis we plan to identify the genes that are differentially expressed during the development of skin carcinoma (SCC) subsquent to the chronic and topical application of a carcinogene agent (DMBA) and a tumor promoter (TPA)
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Project description:WT or Cd226-/- mice were treated with DMBA and TPA. Three weeks later, cells were isolated from mice back skin, and divided CD45+ and CD45- cells by cell sorter. CD45+ and CD45- cells were mixed in 1:1 ratio, and we performed scRNA sequencing of skin cells.
2021-10-26 | GSE174776 | GEO
Project description:We generated meso-scale grids from mouse back skin by collecting paired whole-exome sequencing (WES) and bulk RNA sequencing (bulk RNA), retaining coordinate information to preserve spatial context across the grids. Grids were derived from untreated mice (UN, n = 4), mice treated with the cell-cycle activator TPA for twelve weeks (TO, n = 3), and mice treated with the carcinogen DMBA followed by repeated TPA until the first visible papilloma (DT, n = 3). Cumulatively, we collected 690 bulk RNA and 476 WES samples, the majority of which are paired. All DT animals developed papillomas, whereas no macroscopic skin alterations were observed in UN or TO mice.
2026-06-11 | E-MTAB-15743 | biostudies-arrayexpress
Project description:We generated meso-scale grids from mouse back skin by collecting paired whole-exome sequencing (WES) and bulk RNA sequencing (bulk RNA), retaining coordinate information to preserve spatial context across the grids. Grids were derived from untreated mice (UN, n = 4), mice treated with the cell-cycle activator TPA for twelve weeks (TO, n = 3), and mice treated with the carcinogen DMBA followed by repeated TPA until the first visible papilloma (DT, n = 3). Cumulatively, we collected 690 bulk RNA and 476 WES samples, the majority of which are paired. All DT animals developed papillomas, whereas no macroscopic skin alterations were observed in UN or TO mice.
2026-06-11 | E-MTAB-15745 | biostudies-arrayexpress
Project description:Integrin α3β1 in hair bulge population affects the tumor formation following DMBA/TPA carcinogenesis protocol, however linage tracing showed that hair bulge cells do not largely contributre to tumor mass. To investigate whether α3β1 might affect tumor promoting environment and to better understand its role in hair bulge population during skin tumorigenesis, we determined the expresison profile of hair bulge-originating keratinocytes isolted from α3β1KO and WT mice during initiation of tumorigenesis.
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