ArticleCancer science2010
Oncogenic Ras-mediated downregulation of Clast1/LR8 is involved in Ras-mediated neoplastic transformation and tumorigenesis in NIH3T3 cells.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
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- RORγt+ cells selectively express redundant cation channels linked to the Golgi apparatus.Scientific reports · 2016Article
- Identification of novel targets for antiangiogenic therapy by comparing the gene expressions of tumor and normal endothelial cells.Cancer science · 2014Article
- Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology.Acta histochemica · 2012Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
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Abstract
Oncogenic Ras proteins transform cells by way of multiple downstream signaling pathways that promote the genesis of human cancers. However, the exact cellular mechanisms by which downstream targets are regulated are not fully understood. Here, we show that oncogenic Ras reduced Clast1/LR8 transcript levels in mouse NIH3T3 fibroblasts and human WI38 fibroblasts. Clast1/LR8 transcript was undetectable in H460, A549, and H1299 cells showing high Ras activity, but was relatively abundant in DMS53 cells displaying low Ras activity. We also showed that K-Ras siRNA restored Clast1/LR8 expression in H460 and A549 cells, and that inhibitors of DNA methylation and histone deacetylation reversed oncogenic H-Ras-mediated suppression of Clast1/LR8 transcription. Additionally, ectopic expression of Clast1/LR8 inhibited serum-stimulated phosphorylation of ERK1/2 and Akt in H-RasV12-transformed NIH3T3 cells. We further showed that the expression of Clast1/LR8 interfered with oncogenic Ras-induced NIH3T3 cell transformation and invasion. Finally, our results showed that Clast1/LR8 inhibited Ras-induced proliferation of, and tumor formation by, oncogenic H-RasV12-transformed NIH3T3 cells in vivo. This study identifies the downregulation of Clast1/LR8 as a potentially important mechanism by which oncogenic Ras-mediated neoplastic transformation occurs.
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