ArticleMolecular cancer2013
Epigenetic silencing of RASSF1A deregulates cytoskeleton and promotes malignant behavior of adrenocortical carcinoma.
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The Cytoskeleton in Adrenal Physiology and Tumours: Functional Roles and Emerging Molecular Targets.International journal of molecular sciences · 2025Review
- Wnt/β-catenin signaling pathway in the tumor progression of adrenocortical carcinoma.Frontiers in endocrinology · 2023Review
- Review
- SLC12A7 alters adrenocortical carcinoma cell adhesion properties to promote an aggressive invasive behavior.Cell communication and signaling : CCS · 2018Article
- Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics.Journal of visualized experiments : JoVE · 2018Article
- Methylation markers differentiate thyroid cancer from benign nodules.Journal of endocrinological investigation · 2018Article
- Article
- A novel FOXO1-mediated dedifferentiation blocking role for DKK3 in adrenocortical carcinogenesis.BMC cancer · 2017Article
- Article
- MicroRNA-101 suppresses progression of lung cancer through the PTEN/AKT signaling pathway by targeting DNA methyltransferase 3A.Oncology letters · 2017Article
- Molecular insights into the association of obesity with breast cancer risk: relevance to xenobiotic metabolism and CpG island methylation of tumor suppressor genes.Molecular and cellular biochemistry · 2014Article
- Pathology of the adrenal cortex: a reappraisal of the past 25 years focusing on adrenal cortical tumors.Endocrine pathology · 2014Article
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Authors and funding
7 authors.
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Abstract
backgroundAdrenocortical carcinoma (ACC) is a rare endocrine malignancy with high mutational heterogeneity and a generally poor clinical outcome. Despite implicated roles of deregulated TP53, IGF-2 and Wnt signaling pathways, a clear genetic association or unique mutational link to the disease is still missing. Recent studies suggest a crucial role for epigenetic modifications in the genesis and/or progression of ACC. This study specifically evaluates the potential role of epigenetic silencing of RASSF1A, the most commonly silenced tumor suppressor gene, in adrenocortical malignancy.
resultsUsing adrenocortical tumor and normal tissue specimens, we show a significant reduction in expression of RASSF1A mRNA and protein in ACC. Methylation-sensitive and -dependent restriction enzyme based PCR assays revealed significant DNA hypermethylation of the RASSF1A promoter, suggesting an epigenetic mechanism for RASSF1A silencing in ACC. Conversely, the RASSF1A promoter methylation profile in benign adrenocortical adenomas (ACAs) was found to be very similar to that found in normal adrenal cortex. Enforced expression of ectopic RASSF1A in the SW-13 ACC cell line reduced the overall malignant behavior of the cells, which included impairment of invasion through the basement membrane, cell motility, and solitary cell survival and growth. On the other hand, expression of RASSF1A/A133S, a loss-of-function mutant form of RASSF1A, failed to elicit similar malignancy-suppressing responses in ACC cells. Moreover, association of RASSF1A with the cytoskeleton in RASSF1A-expressing ACC cells and normal adrenal cortex suggests a role for RASSF1A in modulating microtubule dynamics in the adrenal cortex, and thereby potentially blocking malignant progression.
conclusionsDownregulation of RASSF1A via promoter hypermethylation may play a role in the malignant progression of adrenocortical carcinoma possibly by abrogating differentiation-promoting RASSF1A- microtubule interactions.
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