ArticleCancer research2008
Regulation of apoptosis and caspase-8 expression in neuroblastoma cells by isoforms of the IG20 gene.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- IG20/MADD gene functional isoform KIAA0358 can promote insulin secretion in glucose and repaglinide-induced pancreatic β-cells.Acta pharmacologica Sinica · 2026Article
- CRISPR/Cas9-mediated deletion of MADD induces cell cycle arrest and apoptosis in anaplastic thyroid cancer cells.Scientific reports · 2025Article
- A splice site variant in MADD affects hormone expression in pancreatic β cells and pituitary gonadotropes.JCI insight · 2024Article
- Biallelic MADD variants cause a phenotypic spectrum ranging from developmental delay to a multisystem disorder.Brain : a journal of neurology · 2020Article
- Alternative Splicing as a Target for Cancer Treatment.International journal of molecular sciences · 2018Review
- miR-181 interacts with signaling adaptor molecule DENN/MADD and enhances TNF-induced cell death.PloS one · 2017Article
- Alternative splicing as a biomarker and potential target for drug discovery.Acta pharmacologica Sinica · 2015Review
- Article
- MADD is a downstream target of PTEN in triggering apoptosis.Journal of cellular biochemistry · 2014Article
- MADD knock-down enhances doxorubicin and TRAIL induced apoptosis in breast cancer cells.PloS one · 2013Article
- Down-modulation of expression, or dephosphorylation, of IG20/MADD in tumor necrosis factor-related apoptosis-inducing ligand-resistant thyroid cancer cells makes them susceptible to treatment with this ligand.Thyroid : official journal of the American Thyroid Association · 2013Article
- Knockdown of MADD and c-FLIP overcomes resistance to TRAIL-induced apoptosis in ovarian cancer cells.American journal of obstetrics and gynecology · 2011Article
- DENN domain proteins: regulators of Rab GTPases.The Journal of biological chemistry · 2011Review
- Genome-wide analysis of alternative splicing in medulloblastoma identifies splicing patterns characteristic of normal cerebellar development.Cancer research · 2011Article
- Akt-phosphorylated mitogen-activated kinase-activating death domain protein (MADD) inhibits TRAIL-induced apoptosis by blocking Fas-associated death domain (FADD) association with death receptor 4.The Journal of biological chemistry · 2010Article
- MADD, a splice variant of IG20, is indispensable for MAPK activation and protection against apoptosis upon tumor necrosis factor-alpha treatment.The Journal of biological chemistry · 2009Article
- Knockdown of IG20 gene expression renders thyroid cancer cells susceptible to apoptosis.The Journal of clinical endocrinology and metabolism · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The IG20 gene undergoes alternative splicing resulting in the differential expression of six putative splice variants. Four of these (IG20pa, MADD, IG20-SV2, and DENN-SV) are expressed in virtually all human tissues. However, investigations examining alternative splicing of the IG20 gene to date have been largely limited to nonneural malignant and nonmalignant cells. In this study, we investigated the expression of alternative splice isoforms of the IG20 gene in human neuroblastoma cells. We found that six IG20 splice variants (IG20-SVs) were expressed in two human neuroblastoma cell lines (SK-N-SH and SH-SY5Y), highlighted by the expression of two unique splice isoforms (i.e., KIAA0358 and IG20-SV4). Similarly, we found enriched expression of these two IG20-SVs in human neural tissues derived from cerebral cortex, hippocampus, and, to a lesser extent, spinal cord. Using gain-of-function studies and siRNA technology, we determined that these "neural-enriched isoforms" exerted significant and contrasting effects on vulnerability to apoptosis in neuroblastoma cells. Specifically, expression of KIAA0358 exerted a potent antiapoptotic effect in both the SK-N-SH and SH-SY5Y neuroblastoma cell lines, whereas expression of IG20-SV4 had proapoptotic effects directly related to the activation of caspase-8 in these cells, which have minimal or absent constitutive caspase-8 expression. These data indicate that the pattern of expression of these neural-enriched IG20-SVs regulates the expression and activation of caspase-8 in certain neuroblastoma cells, and that manipulation of IG20-SV expression pattern may represent a potent therapeutic strategy in the therapy of neuroblastoma and perhaps other cancers.
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Registered trials
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