ArticleCancer research2009
Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Unveiling PANoptosis in Acute Kidney Injury: An Integrative Multi-Dimensional Approach to Identify Key Biomarkers.Journal of inflammation research · 2025Article
- Knowledge mapping of anaplastic thyroid cancer treatments: a bibliometric analysis (2000-2023).Frontiers in oncology · 2024Article
- S100PBP is regulated by mutated KRAS and plays a tumour suppressor role in pancreatic cancer.Oncogene · 2023Article
- Review
- Identification of potential microRNA panels for pancreatic cancer diagnosis using microarray datasets and bioinformatics methods.Scientific reports · 2020Article
- Rho guanine nucleotide exchange factor ARHGEF10 is a putative tumor suppressor in pancreatic ductal adenocarcinoma.Oncogene · 2020Article
- Novel treatments for anaplastic thyroid carcinoma.Gland surgery · 2020Review
- Regulation of RhoB Gene Expression during Tumorigenesis and Aging Process and Its Potential Applications in These Processes.Cancers · 2019Review
- The RhoB small GTPase in physiology and disease.Small GTPases · 2018Review
- The PPARγ agonist efatutazone delays invasive progression and induces differentiation of ductal carcinoma in situ.Breast cancer research and treatment · 2018Article
- Evolving molecularly targeted therapies for advanced-stage thyroid cancers.Nature reviews. Clinical oncology · 2016Review
- Peroxisome proliferator-activated receptor-γ agonist inhibits collagen synthesis in human keloid fibroblasts by suppression of early growth response-1 expression through upregulation of miR-543 expression.American journal of cancer research · 2016Article
- RETRACTED: RhoB Acts as a Tumor Suppressor That Inhibits Malignancy of Clear Cell Renal Cell Carcinoma.PloS one · 2016Article
- RhoB upregulation leads to either apoptosis or cytostasis through differential target selection.Endocrine-related cancer · 2015Article
- Article
- New therapies for dedifferentiated papillary thyroid cancer.International journal of molecular sciences · 2015Review
- The neddylation-cullin 2-RBX1 E3 ligase axis targets tumor suppressor RhoB for degradation in liver cancer.Molecular & cellular proteomics : MCP · 2015Article
- Molecular Targeted Therapies of Aggressive Thyroid Cancer.Frontiers in endocrinology · 2015Review
- Personalization of targeted therapy in advanced thyroid cancer.Current genomics · 2014Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Anaplastic thyroid carcinoma (ATC) is a highly aggressive form of the disease for which new therapeutic options are desperately needed. Previously, we showed that the high-affinity peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, RS5444, inhibits cell proliferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21). We show here that up-regulation of RhoB is a critical step in PPARgamma-mediated activation of p21-induced cell stasis. Using multiple independently derived ATC cell lines, we found that treatment with RS5444 leads to the up-regulation of RhoB and subsequent activation of p21, and that silencing of RhoB by RNAi blocks the ability of RS5444 to induce p21 and to inhibit cell proliferation. Our results show that transcriptional regulation of RhoB by the nuclear transcription factor PPARgamma is responsible for the induction of p21 mRNA and protein. We further implicate RhoB as a key signaling effector for the growth inhibition of ATC, as treatment with a histone deacetylase inhibitor shown to increase RhoB expression in lung cancer cells caused the up-regulation of RhoB in ATC cells accompanied by increased expression of p21 and inhibition of cell proliferation; this effect occurred even in ATC cells that were unresponsive to RS5444 due to a lack of expression of PPARgamma. Our results implicate RhoB as a novel intermediate in critical signaling pathways and as an additional target for therapeutic intervention in ATC.
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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.