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 cilia play a role in metabolic reprogramming in thyroid cancer cells.