Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0

A novel EMT-selective small molecule induces ER stress

ABSTRACT: Carcinoma cells can acquire key malignant traits by reprogramming their differentiation state via an epithelial-to-mesenchymal transition (EMT). Cancer cells that undergo EMT become invasive and resist a wide range of therapies including most chemotherapy drugs and radiation. Such cells are also able to efficiently seed primary and metastatic tumors, making them functionally indistinguishable from tumor-initiating or cancer stem-like cells (TICs or CSCs). Therefore, there is significant interest in finding vulnerabilities of cancer cells that have undergone EMT. A potent EMT-selective small molecule was discovered through a large-scale chemical screen. We used microarray analysis to understand the biological effects of this compound. HMLE_ctrl (human MECs, infected with a pBabe-shGFP retrovirus) and HMLE_Twist (human MECs, infected with a pBabe-Twist retrovirus) cells were treated with solvent control (DMSO), 5 µM or 10 µM of Cmp302 for 6 hours. Microarray analysis was performed to profile global gene expression.

ORGANISM(S): Homo sapiens

SUBMITTER: Yu-xiong Feng 

PROVIDER: E-GEOD-55604 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

Json Xml
altmetric image

Publications

Epithelial-to-mesenchymal transition activates PERK-eIF2α and sensitizes cells to endoplasmic reticulum stress.

Feng Yu-Xiong YX   Sokol Ethan S ES   Del Vecchio Catherine A CA   Sanduja Sandhya S   Claessen Jasper H L JH   Proia Theresa A TA   Jin Dexter X DX   Reinhardt Ferenc F   Ploegh Hidde L HL   Wang Qiu Q   Gupta Piyush B PB  

Cancer discovery 20140404 6

<h4>Unlabelled</h4>Epithelial-to-mesenchymal transition (EMT) promotes both tumor progression and drug resistance, yet few vulnerabilities of this state have been identified. Using selective small molecules as cellular probes, we show that induction of EMT greatly sensitizes cells to agents that perturb endoplasmic reticulum (ER) function. This sensitivity to ER perturbations is caused by the synthesis and secretion of large quantities of extracellular matrix (ECM) proteins by EMT cells. Consist  ...[more]

Similar Datasets

Transcriptomics Impact of BHLHE40-AS1 over expression in MCF10A cells
2020-06-10 | GSE136579 | GEO
Transcriptomics The dynamics of chromatin accessibility during EMT
2015-12-31 | E-GEOD-63366 | biostudies-arrayexpress
Transcriptomics MET after transient Twist activation results in de novo gain of malignant traits
2015-07-02 | E-GEOD-61206 | biostudies-arrayexpress
no omics defined Transcription profiling of mouse Deaf-1-transduced mammary epithelial cells
2008-10-25 | E-GEOD-12367 | biostudies-arrayexpress
Transcriptomics RNA-seq of two human mammary epithelial cell lines (HMLE and HMLE-Twist-ER) treated with 4-hydroxytamoxifen vs control
2021-03-24 | E-MTAB-9365 | biostudies-arrayexpress
Transcriptomics Mutation of GATA3 in Human Breast Tumors
2004-05-24 | GSE841 | GEO
Transcriptomics An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype.
2011-07-15 | E-GEOD-30290 | biostudies-arrayexpress
Transcriptomics Network Understanding of SNAIL inhibitor induced perturbations in EMT models
2013-05-31 | E-GEOD-44397 | biostudies-arrayexpress
Transcriptomics The microRNA profile analysis of the function of HMGA2 in immortalized human ovarian surface epithelial cell lines
2010-09-11 | E-GEOD-23634 | biostudies-arrayexpress
Transcriptomics Effect of NF-kB inhibition and activation on gene expression in mouse and human lung cancer cell-lines
2013-05-01 | E-GEOD-44619 | biostudies-arrayexpress