Literature DB >> 19190106

Knockdown of IG20 gene expression renders thyroid cancer cells susceptible to apoptosis.

Mahesh Subramanian1, Tania Pilli, Palash Bhattacharya, Furio Pacini, Yuri E Nikiforov, Prasad V Kanteti, Bellur S Prabhakar.   

Abstract

AIM: The aim of the study was to investigate the expression and function of the IG20 gene in thyroid cancer cell survival, proliferation, and apoptosis.
METHODS: We 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.
RESULTS: The 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.
CONCLUSION: IG20 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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Year:  2009        PMID: 19190106      PMCID: PMC2682475          DOI: 10.1210/jc.2008-2378

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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