Publication: The tumor suppressor RASSF1A in human carcinogenesis: an update
Authors
Dammann, R. ; Schagdarsurengin, U. ; Seidel, C. ; Strunnikova, M. ; Rastetter, M. ; Baier, K. ; Pfeifer, G.P.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Loss of heterozygosity of the small arm of
chromosome 3 is one of the most common alterations in
human cancer. Most notably, a segment in 3p21.3 is
frequently lost in lung cancer and several other
carcinomas. We and others have identified a novel Ras
effector at this segment, which was termed Ras
Association Domain family 1 (RASSF1A) gene.
RASSF1 consists of two main variants (RASSF1A and
RASSF1C), which are transcribed from distinct CpG
island promoters. Aberrant methylation of the RASSF1A
promoter region is one of the most frequent epigenetic
inactivation events detected in human cancer and leads
to silencing of RASSF1A. Hypermethylation of
RASSF1A was commonly observed in primary tumors
including lung, breast, pancreas, kidney, liver, cervix,
nasopharyngeal, prostate, thyroid and other cancers.
Moreover, RASSF1A methylation was frequently
detected in body fluids including blood, urine, nipple
aspirates, sputum and bronchial alveolar lavages.
Inactivation of RASSF1A was associated with an
advanced tumor stage (e.g. bladder, brain, prostate,
gastric tumors) and poor prognosis (e.g. lung, sarcoma
and breast cancer). Detection of aberrant RASSF1A
methylation may serve as a diagnostic and prognostic marker. The functional analyses of RASSF1A reveal an
involvement in apoptotic signaling, microtubule
stabilization and mitotic progression. The tumor
suppressor RASSF1A may act as a negative Ras effector
inhibiting cell growth and inducing cell death. Thus,
RASSF1A may represent an epigenetically inactivated
bona fide tumor suppressor in human carcinogenesis.
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