Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nanolipoprotein mediated Her2 protein transfection induces malignant transformation in human breast acinar cultures

ABSTRACT: We describe transcriptomic changes in HMT-3522-S1 cells cultured in the acinar morphogenesis assay in reponse to either empty-nanolipoprotein stimulus, Her2-nanolipoprotien stimulus or control unstimulated cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184648 | GEO | 2021/11/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nanolipoprotein-Mediated Her2 Protein Transfection Induces Malignant Transformation in Human Breast Acinar Cultures.

Project description:Her2 overexpression is associated with an aggressive form of breast cancer and malignant transformation. We demonstrate in this work that nanolipoprotein particles (NLPs) synthesized in a cell-free manner can be used to transfer Her2 protein into the membrane of nonmalignant cells in 3D culture in a nontoxic and facile manner. With NLP-mediated Her2 protein delivery, we observed an increased probability of nonmalignant cells forming apolar nongrowth-arrested tumor-like structures. The NLP delivery system alone or Her2-NLPs plus the Her2 inhibitor trastuzumab showed no effect on the acinar organization rate, indicating that Her2 signaling is key to this process. Transcriptomics revealed essentially no effect of empty NLPs compared to untreated cells, whereas Her2-NLPs versus either untreated or empty-NLP-treated cells revealed upregulation of several factors associated with breast cancer. Pathway analysis also suggested that known nodes downstream of Her2 were activated in response to Her2-NLP treatment. This demonstrates that Her2 protein delivery with NLPs is sufficient for the malignant transformation of nonmalignant cells. Thus, this system offers a new model for studying cell surface receptor signaling without genomic modification or transformation techniques.

| S-EPMC8581977 | biostudies-literature

Nanolipoprotein mediated Her2 protein transfection induces malignant transformation in human breast acinar cultures

Project description:Nanolipoprotein mediated Her2 protein transfection induces malignant transformation in human breast acinar cultures

| PRJNA765587 | ENA

RNA-Seq of explanted murine pancreatic acinar cells

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia, pancreatic acinar cells were isolated from 5 week old KrasG12D-mice. RNA was isolated immediately after isolation (t=0 days) or after 3 days embedded in collagen.

2023-03-02 | E-MTAB-9878 | biostudies-arrayexpress

Proteogenomic characterization of pancreatic acinar cell carcinoma and pancreatoblastoma

Project description:To characterize pancreatic cancer with acinar differentiation at protein level, we performed mass spectromery-based proteome analysis using clinical FFPE tissue samples.

2024-09-17 | PXD036998 | Pride

Gene expression of non-apoptotic pancreatic acinar cell death with autophagy

Project description:Serine protease inhibitor Kazal type 3 (Spink3) is a trypsin inhibitor in the pancreas. Spink3-/- pancreatic acinar cells are dead with excessive autophagy at birth (p0.5). To prove the role of nonapoptotic cell death with autophagy, we generated by transgenic technology the pancreas of Spink3-/-;XKI/+ mice contained both normal and dying acinar cells with autophagy. In this new mouse model, chronic inflammation occurred in the pancreas, indicating that some signals from nonapoptotic dead cell induce chronic inflammation in the pancreas. All samples were the pancreas at p0.5. Sample 1 and 2 are the pancreas from wild type (Spink3+/+, control) mice. Sample 3 and 4 are the pancreas from Spink3-/-, which all pancreatic acinar cells show induced nonapoptotic cell death with autophagy. Sample 5 and 6 are the pancreas from Spink3-/-XKI/+, about half acinar cells are normal, but other acinar cells show induced nonapoptotic cell death with autophagy.

2016-07-16 | E-GEOD-48946 | biostudies-arrayexpress

c-Myc down-regulation is required for pre-acinar to acinar maturation in the pancreas (RNA-Seq)

Project description:Multipotent pancreatic progenitors (MPC) are defined as Ptf1a+, Mychigh, Cpa+ cells. During the transition from MPC to unipotent acinar progenitors, c-Myc is down-regulated whereas Ptf1a is up-regulated, leading to the deployment of the acinar program. Here, we show that c-Myc and Ptf1a interact directly and c-Myc binds to, and represses, the transcriptional activity of the PTF1 complex in vitro and in vivo. Using Ela1-Myc mice, in which c-Myc is overexpressed in acinar cells starting at E14.5, we find that acinar cells fail to undergo normal maturation at P1 and this is followed by a massive subsequent repression of the acinar programme. Lineage tracing with Ptf1aCreERT2;Rosa26YFP and Ela1-Myc;Ptf1aCreERT2;Rosa26YFP mice receiving TMX at E15.5 and analyzed at E18.5 revealed that c-Myc overexpression is associated with activation of a hepatic programme but not with pancreatic lineage misspecification At 8 weeks, the silencing of the acinar program is associated with increased expression of the PRC2 complex in a c-Myc dependent manner. Genome wide studies show that Ptf1a and c-Myc display partially overlapping chromatin occupancy patterns and DNA binding competition. We conclude that c-Myc down-regulation during development is crucial for the maturation of pre-acinar to acinar cells. c-Myc overexpression may contribute to pancreatic carcinogenesis by restraining cell differentiation and rendering cells susceptible to transformation.

2017-12-11 | GSE77410 | GEO

c-Myc down-regulation is required for pre-acinar to acinar maturation in the pancreas (ChIP-Seq)

2017-12-11 | GSE77409 | GEO

Homo sapiens

Project description:Homo sapiens HMT-3522 S1 transcriptome - S1 IR_II

| PRJNA458039 | ENA

Homo sapiens

Project description:Homo sapiens HMT-3522 S1 transcriptome - S1 IR_III

| PRJNA458040 | ENA

Homo sapiens

Project description:Homo sapiens HMT-3522 S1 transcriptome - S1 sham_I

| PRJNA458026 | ENA