ArticleOncogene2004
Transcriptional basis of KRAS oncogene-mediated cellular transformation in ovarian epithelial cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 76 citations in OpenAlex.
- Spontaneously evolved progenitor niches escape Yap oncogene addiction in advanced pancreatic ductal adenocarcinomas.Nature communications · 2023Article
- Role of the Transcription Factor FOSL1 in Organ Development and Tumorigenesis.International journal of molecular sciences · 2022Review
- Targeting K-Ras and apoptosis-driven cellular transformation in cancer.Cell death discovery · 2021Review
- Reduced replication origin licensing selectively kills KRAS-mutant colorectal cancer cells via mitotic catastrophe.Cell death & disease · 2020Article
- The brain acid-soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin.Molecular oncology · 2020Article
- Expression and function of FRA1 protein in tumors.Molecular biology reports · 2020Review
- A Unique Family of Neuronal Signaling Proteins Implicated in Oncogenesis and Tumor Suppression.Frontiers in oncology · 2019Review
- Establishment and characterization of novel human primary endometrial cancer cell line (ZJB-ENC1) and its genomic characteristic.Journal of Cancer · 2019Article
- Arsenite malignantly transforms human prostate epithelial cells in vitro by gene amplification of mutated KRAS.PloS one · 2019Article
- An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.Nature communications · 2017Article
- Effects of RAL signal transduction in KRAS- and BRAF-mutated cells and prognostic potential of the RAL signature in colorectal cancer.Oncotarget · 2015Article
- Differential reprogramming of isogenic colorectal cancer cells by distinct activating KRAS mutations.Journal of proteome research · 2015Article
- Identification of mutant K-Ras-dependent phenotypes using a panel of isogenic cell lines.The Journal of biological chemistry · 2013Article
- Label-free quantitative proteomics and N-glycoproteomics analysis of KRAS-activated human bronchial epithelial cells.Molecular & cellular proteomics : MCP · 2012Article
- HER-2/neu-mediated down-regulation of biglycan associated with altered growth properties.The Journal of biological chemistry · 2012Article
- Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS.Molecular systems biology · 2012Article
- Identification of Y-box binding protein 1 as a core regulator of MEK/ERK pathway-dependent gene signatures in colorectal cancer cells.PLoS genetics · 2010Article
- Atypical protein kinase C{iota} is required for bronchioalveolar stem cell expansion and lung tumorigenesis.Cancer research · 2009Article
- Let-7 and miR-200 microRNAs: guardians against pluripotency and cancer progression.Cell cycle (Georgetown, Tex.) · 2009Review
- Overexpressed vs mutated Kras in murine fibroblasts: a molecular phenotyping study.British journal of cancer · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand the relationship between oncogenic signaling and the reprogramming of gene expression, we performed transcriptional profiling in rat ovarian surface epithelial cells (ROSE), in which neoplastic transformation is driven by a mutated KRAS oncogene. We identified >200 genes whose expression was elevated or reduced following permanent KRAS expression. Deregulated KRAS-responsive genes encode transcriptional regulators, signaling effectors, proteases, extracellular matrix and adhesion proteins, transformation-suppressing proteins and negative growth regulators. Many of them have not been previously identified in cells expressing oncogenic RAS genes or in other well-studied models of oncogenic signaling. The number of critical genes related to the execution of anchorage-independent proliferation and epithelial-mesenchymal transition was narrowed down to 79 by selectively inhibiting the mitogen-activated protein kinase (MAPK/ERK) and phosphatidylinositol 3-kinase (PI3K) pathways. Blocking MAPK/ERK-signaling caused reversion to the normal epithelial phenotype in conjunction with the reversal of deregulated target transcription to pretransformation levels. In addition, silencing of the overexpressed transcriptional regulator Fra-1 by RNA interference resulted in growth reduction, suggesting that this factor partially contributes to, but is not sufficient for the proliferative capacity of KRAS-transformed epithelial cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.