ArticleBreast cancer research and treatment2009
Immortalization and transformation of human mammary epithelial cells by a tumor-derived Myc mutant.
Article in Breast cancer research and treatment, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- MYC-driven gliosis impairs neuron-glia communication in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- T-cell Dysfunction upon Expression of MYC with Altered Phosphorylation at Threonine 58 and Serine 62.Molecular cancer research : MCR · 2022Article
- Establishment and characterization of immortalized sweat gland myoepithelial cells.Scientific reports · 2022Article
- Article
- Profound Reprogramming towards Stemness in Pancreatic Cancer Cells as Adaptation to AKT Inhibition.Cancers · 2020Article
- MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer.British journal of cancer · 2020Article
- p53-independent role of MYC mutant T58A in the proliferation and apoptosis of breast cancer cells.Oncology letters · 2019Article
- Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells.BioMed research international · 2018Article
- ROCK inhibitor reduces Myc-induced apoptosis and mediates immortalization of human keratinocytes.Oncotarget · 2016Article
- Article
- Expression of RUNX1 correlates with poor patient prognosis in triple negative breast cancer.PloS one · 2014Article
- HMGA1: a master regulator of tumor progression in triple-negative breast cancer cells.PloS one · 2013Article
- Mechanistic insight into Myc stabilization in breast cancer involving aberrant Axin1 expression.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- ROCK inhibitor and feeder cells induce the conditional reprogramming of epithelial cells.The American journal of pathology · 2012Article
- Phosphorylation regulates c-Myc's oncogenic activity in the mammary gland.Cancer research · 2011Article
- Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.Cell cycle (Georgetown, Tex.) · 2011Review
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The Myc transcription factor is commonly dysregulated in many human cancers, including breast carcinomas. However, the precise role of Myc in the initiation and maintenance of malignancy is unclear. In this study we compared the ability of wild-type Myc (wt Myc) or Myc phosphorylation deficient mutants (T58A, S62A or T58A/S62A) to immortalize and transform human mammary epithelial cells (HMECs). All Myc constructs promoted cellular immortalization. As previously reported in other cells, the Myc T58A mutant tempered apoptotic responses and increased Myc protein stability in HMEC cells. More importantly, we now show that HMECs overexpressing the Myc T58A mutant acquire a unique cellular phenotype characterized by cell aggregation, detachment from the substrate and growth in liquid suspension. Coincident with these changes, the cells become anchorage-independent for growth in agarose. Previous studies have shown that wt Myc can collaborate with hTERT in inducing HMEC anchorage-independent growth. We have verified this observation and further shown that Myc T58A was a stronger facilitator of such co-transformation. Thus, our findings indicate that differences in Myc protein phosphorylation modulate its biological activity in human breast epithelial cells and specifically that the T58A mutation can facilitate both cellular immortalization and transformation. Finally, we used the isogenic cell lines generated in this study to identify a subset of genes whose expression is greatly altered during the transition from the immortal to the anchorage-independent states.
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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.