ArticleJournal of cancer research and clinical oncology2007
Pro-apoptotic activity of oncogenic H-Ras for histone deacetylase inhibitor to induce apoptosis of human cancer HT29 cells.
Article in Journal of cancer research and clinical oncology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- What we have learnt fromHeliyon · 2022Review
- A triple combination gemcitabine + romidepsin + cisplatin to effectively control triple-negative breast cancer tumor development, recurrence, and metastasis.Cancer chemotherapy and pharmacology · 2021Article
- Compensatory combination of romidepsin with gemcitabine and cisplatin to effectively and safely control urothelial carcinoma.British journal of cancer · 2020Article
- Reactive oxygen species-mediated therapeutic control of bladder cancer.Nature reviews. Urology · 2011Review
- Differential induction of reactive oxygen species through Erk1/2 and Nox-1 by FK228 for selective apoptosis of oncogenic H-Ras-expressing human urinary bladder cancer J82 cells.Journal of cancer research and clinical oncology · 2011Article
- Molecular genesis of non-muscle-invasive urothelial carcinoma (NMIUC).Expert reviews in molecular medicine · 2010Review
- Role of reactive oxygen species in proapoptotic ability of oncogenic H-Ras to increase human bladder cancer cell susceptibility to histone deacetylase inhibitor for caspase induction.Journal of cancer research and clinical oncology · 2009Article
- Romidepsin inhibits Ras-dependent growth transformation of NIH 3T3 fibroblasts and RIE-1 epithelial cells independently of Ras signaling inhibition.Journal of molecular signaling · 2009Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo verify the pro-apoptotic activity of oncogenic H-Ras in the increased susceptibility of human cancer cells to histone deacetylase inhibitor (HDACI).
methodsThe pro-apoptotic activity of oncogenic H-Ras(V12) was verified by its ability to increase susceptibility of human colorectal adenocarcinoma HT29 cells to HDACI for inducing apoptosis and growth inhibition, assayed by various methods. The mode of action of HDACI FR901228 was studied by its ability to modulate protein phosphorylation, acetylation, and expression levels in various signaling pathways, measured by Western blot analysis.
resultsActivation of caspase-3, -7, and -8, and serine protease by FR901228 was facilitated by oncogenic H-Ras to induce apoptosis. Expression of H-Ras(V12) changed the intrinsic modulation of Raf in cells responding to FR901228 treatment. Both p21( Cip1 ) and p27( Kip1 ) were induced in FR901228-treated cells arrested in either the G0/G1 or G2/M phase of the cell cycle. Deacetylation of FR901228-induced acetylation of core histones was accelerated by H-Ras(V12) in cells undergoing apoptosis.
conclusionExpression of H-Ras(V12) increased susceptibility of HT29 cells to HDACI FR901228 and Trichostatin A for inducing apoptosis. The pro-apoptotic activity of H-Ras(V12) responding to HDACI indicates a potential value of this new class of anticancer agents in treating Ras-related human cancers.
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