ArticleOncotarget2015
Loss of β-catenin in adrenocortical cancer cells causes growth inhibition and reversal of epithelial-to-mesenchymal transition.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- (Non)canonical Wnt signaling, cytoarchitecture and stemness: new insights from primary nonmetastatic, primary metastatic, regional and distant metastatic models of adrenocortical carcinoma.Experimental & molecular medicine · 2025Article
- A reappraisal of transcriptional regulation by NR5A1 and beta-catenin in adrenocortical carcinoma.Frontiers in endocrinology · 2023Article
- Preclinical assessment of synergistic efficacy of MELK and CDK inhibitors in adrenocortical cancer.Journal of experimental & clinical cancer research : CR · 2022Article
- Review
- Inhibition of Aurora kinase A activity enhances the antitumor response of beta-catenin blockade in human adrenocortical cancer cells.Molecular and cellular endocrinology · 2021Article
- A novel heat shock protein 90 inhibitor potently targets adrenocortical carcinoma tumor suppression.Surgery · 2020Article
- microRNA-431 as a Chemosensitizer and Potentiator of Drug Activity in Adrenocortical Carcinoma.The oncologist · 2019Article
- Article
- A Novel TP53 Mutation Associated with TWIST1 and SIP1 Expression in an Aggressive Adrenocortical Carcinoma.Endocrine pathology · 2017Article
- Article
- Article
- Article
- Cell signaling pathways in the adrenal cortex: Links to stem/progenitor biology and neoplasia.Molecular and cellular endocrinology · 2017Review
- Article
- NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation.Oncology letters · 2017Article
- Identification of Niclosamide as a Novel Anticancer Agent for Adrenocortical Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- 5th International ACC Symposium: An Outlook to Current and Future Research on the Biology of Adrenocortical Carcinoma: Diagnostic and Therapeutic Applications.Hormones & cancer · 2016Review
- Sphingosine kinase 1 is overexpressed and promotes adrenocortical carcinoma progression.Oncotarget · 2016Article
- Senescence Process in Primary Wilms' Tumor Cell Culture Induced by p53 Independent p21 Expression.Journal of Cancer · 2016Article
- The PI3K/Akt Pathway in Tumors of Endocrine Tissues.Frontiers in endocrinology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adrenal carcinoma (ACC) is a rare neoplasm with a poor outcome. Aberrant expression of β-catenin has been found in approximatively 30% of ACC. We herein studied its effects on the growth of the human ACC cell line H295R. The cells were infected with short hairpin RNA (shRNA)-mediated silencing β-catenin. Two shRNAs used induced down-regulation of β-catenin protein levels. The expression of these shRNAs decreased cell growth and increased H295R cells in S and G2/M phases. This cytostatic effect is due to a decrease of phosphorylated MAPK and to an up-regulation expression of the cyclin-dependent kinase inhibitors p57(KIP2), p21(CIP) and p27(KIP1). In addition, the knockdown of β-catenin decreased phosphorylated Akt and increased apoptosis. Finally, loss of β-catenin was sufficient to induce the reversal of the epithelial-to-mesenchymal transition. We then transplanted these genetically modified H295R cells in Scid mice. Tumor growth suppression was achieved by the two shRNAs showing in vitro efficacy. Proliferation was not reduced in silenced tumors. In contrast, p57, p27 and p21 proteins were found expressed at high levels in silenced tumors along with an increase in apoptotic cells. These findings indicate that β-catenin loss in H295R cells inhibits tumor growth by inducing transcriptional and functional changes.
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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.