ArticleThe Journal of clinical endocrinology and metabolism2009
Knockdown of IG20 gene expression renders thyroid cancer cells susceptible to apoptosis.
Article in The Journal of clinical endocrinology and metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- CRISPR/Cas9-mediated deletion of MADD induces cell cycle arrest and apoptosis in anaplastic thyroid cancer cells.Scientific reports · 2025Article
- Review
- Vemurafenib may overcome TNF-related apoptosis-inducing ligand (TRAIL) resistance in anaplastic thyroid cancer cells.Endocrine · 2020Article
- Loss of MADD expression inhibits cellular growth and metastasis in anaplastic thyroid cancer.Cell death & disease · 2019Article
- miR-181 interacts with signaling adaptor molecule DENN/MADD and enhances TNF-induced cell death.PloS one · 2017Article
- Article
- 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
- 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
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
aimThe aim of the study was to investigate the expression and function of the IG20 gene in thyroid cancer cell survival, proliferation, and apoptosis.
methodsWe determined the expression levels of the major isoforms of IG20 by quantitative RT-PCR in normal and thyroid tumor tissues/cell lines. We evaluated the functional consequence of IG20 knockdown in WRO (follicular carcinoma) and FRO (anaplastic carcinoma) thyroid cancer cell lines by measuring spontaneous, TNFalpha-related apoptosis-inducing ligand (TRAIL), and TNFalpha-induced apoptosis.
resultsThe IG20 gene expression levels were higher in benign and malignant thyroid tumors and in WRO and FRO cells relative to normal tissues. Predominantly, MADD and DENN-SV isoforms of IG20 gene were expressed. IG20 knockdown resulted in increased spontaneous, TRAIL-, and TNFalpha-induced apoptosis in WRO, but not FRO, cells. FRO cell resistance to apoptosis is likely due to caspase-8 deficiency.
conclusionIG20 knockdown renders WRO cells more susceptible to spontaneous, TRAIL-, and TNFalpha-induced apoptosis and thus demonstrates the prosurvival function of the IG20 gene in thyroid cancer. These observations, combined with overexpression of IG20 noted in thyroid tumor tissues, may suggest a potential role in thyroid cancer survival and growth and indicate that IG20 may be targeted either alone or in conjunction with TRAIL or TNFalpha treatment in certain thyroid cancers.
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