Loss-of-function of IFT88 determines metabolic phenotypes in thyroid cancer

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Primary cilia are microtubule-based, dynamic organelles characterized by continuous assembly and disassembly. The intraflagellar transport (IFT) machinery, including IFT88 in cilia, is involved in the maintenance of bidirectional motility along the axonemes, which is required for ciliogenesis and functional competence. Cancer cells are frequently associated with loss of primary cilia and IFT functions. However, there is little information on the role of IFT88 or primary cilia in the metabolic remodeling of cancer cells. Therefore, we investigated the cellular and metabolic effects of the loss-of-function (LOF) mutations of IFT88/primary cilia in thyroid cancer cells. IFT88-deficient 8505C thyroid cancer cells were generated using the CRISPR/Cas9 system, and RNA-sequencing analysis was performed. LOF of the IFT88 gene resulted in a marked defect in ciliogenesis and mitochondrial oxidative function. Gene expression patterns in IFT88-deficient thyroid cancer cells favored glycolysis and lipid biosynthesis. However, LOF of IFT88/primary cilia did not promote thyroid cancer cell proliferation, migration, and invasion. The results suggest that IFT88/primary mary cilia play a role in metabolic reprogramming in thyroid cancer cells.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2018-08
Language
English
Article Type
Article
Keywords

INTRAFLAGELLAR TRANSPORT PROTEINS; CYSTIC KIDNEY-DISEASE; BARDET-BIEDL-SYNDROME; PRIMARY CILIA; TUMOR SUPPRESSORS; GENE TG737; SENESCENCE; COMPLEX; AURORA; CELLS

Citation

ONCOGENE, v.37, no.32, pp.4455 - 4474

ISSN
0950-9232
DOI
10.1038/s41388-018-0211-6
URI
http://hdl.handle.net/10203/245404
Appears in Collection
MSE-Journal Papers(저널논문)
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