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Next-generation sequencing analysis of control mammary glands and ECD transgenic tumors

ABSTRACT: Overexpression of ECD in mammary gland promotes mammary tumorigenesis. To determine the plausible mechanism of how ECD contributes the oncogenesis, we performed RNAseq analysis of three independent control mice mammary glands (6 months old) and four independent ECD transgenic mammary tumors. Out of these four tumors, T1a and T1b were adenosquamous carcinoma type, T3 was Spindle cell carcinoma type and T4 was papillary carcinoma. RNA was isolated from the respective samples and RNAseq was performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE200838 | GEO | 2022/05/18

REPOSITORIES: GEO

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Pancreatic Cancer HPAF/CD18 cells: Ecd knockdown vs Scrambled

Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells. Two-condition experiment, Ecd knockdown vs Scrambled cells. Biological replicates: 3 Ecd knockdownl, 3 Scrambled, independently grown and harvested. One replicate per array

2012-08-09 | E-GEOD-39988 | biostudies-arrayexpress

Pancreatic Cancer HPAF/CD18 cells: Ecd knockdown vs Scrambled

2012-08-10 | GSE39988 | GEO

Next-generation sequencing analysis of control mammary glands and ECD transgenic tumors

Project description:Next-generation sequencing analysis of control mammary glands and ECD transgenic tumors

| PRJNA826889 | ENA

Response of C2C12-hN1∆ECD to DAPT washout

Project description:C2C12 cells expressing constitutively active hN1∆ECD were activated by complete DAPT washout for 1h or 6h, or left in 10 uM DAPT

2016-09-04 | GSE72847 | GEO

Loss of c-Jun NH2-Terminal Kinase in Mammary Epithelial Cells is Sufficient for Adenosquamous Tumor Formation

Project description:The JNK pathway has been implicated in breast cancer, both from human tumor sequencing studies and from mouse models. To see if JNK deletion is able to form tumors in mice, we crossed Mapk8 and Mapk9 conditional animals with the WAP-Cre expressing mouse to specifically delete JNK in luminal epithelial cells of the breast. We found that JNK suppresses tumors and that the loss of JNK leads to adenosquamous carcinoma formation. To understand the role of JNK in the mammary epithelium, we performed RNA sequencing and analyzed gene expression from tumor-derived cell lines. Several pathways were perturbed in the carcinoma cell lines. Our results demonstrate that loss of JNK alone is sufficient to cause tumor formation and they reveal a gene signature of adenosquamous tumors that can help in better understanding and treating the disease.

2018-05-29 | GSE100581 | GEO

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Ecd protein interactome in Drosophila melanogaster S2 cells

Project description:Identification of the interaction partners of the protein ecdysoneless (Ecd) in Drosophila melanogaster S2 cells as well as profiling of the changes in binding for mutant, truncated Ecd del34 protein.

2021-09-09 | PXD019838 | Pride

Comprehensive profile and contrastive analysis of circular RNA in cervical squamous carcinoma and adenocarcinoma

Project description:To contrastively analyze the expression pattern of circRNAs in cervical squamous carcinoma, adenocarcinoma and adenosquamous carcinoma variants. CircRNAs expression in cervical squamous carcinoma, adenocarcinoma and adenosquamous carcinoma tissues together with the adjacent normal tissues were profiled by high-throughput RNA sequencing.

2022-12-31 | GSE208089 | GEO

Tumor T4 Sectors

Project description:The following CGH experiments were conducted on four sectors (S1-S4) from a single primary ductal carcinoma tumor (T4).

2009-07-10 | GSE16601 | GEO

Sym004 in Metastatic Colorectal Cancer and ECD-EGFR Patients

Project description:This is a single arm, phase 2, open-label, multicenter trial in patients with metastatic colorectal cancer (mCRC) and acquired resistance to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) and documented mutation of extra cellular domain EGFR (ECD-EGFR).

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