Evidence map›Paper›PMID 29743590›Full record

ArticleOncogene2018

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

Junguee Lee, Shinae Yi, Minho Won, Young Shin Song, Hyon-Seung Yi, Young Joo Park, Ki Cheol Park, Jung Tae Kim, Joon Young Chang, Min Joung Lee and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  6. Article
  7. International journal of molecular sciences · 2024
    Article
  8. The role of primary cilia in the testis.Current opinion in endocrine and metabolic research · 2024
    Article
  9. Article
  10. Article
  11. The role of primary cilia in thyroid diseases.Frontiers in endocrinology · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 2 countries.

Junguee LeeDepartment of Pathology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, 34943, Republic of Korea.
Shinae YiResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Minho WonDepartment of Pharmacology, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Young Shin SongDepartment of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Hyon-Seung YiResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Young Joo ParkDepartment of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Ki Cheol ParkClinical Research Institute, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, 34943, Republic of Korea.
Jung Tae KimResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Joon Young ChangResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Min Joung LeeDepartment of Biochemistry, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Hae Joung SulDepartment of Pathology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, 34943, Republic of Korea.
Ji Eun ChoiDepartment of Pathology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 64 Daeheung-ro, Jung-gu, Daejeon, 34943, Republic of Korea.
Koon Soon KimResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea.
Jukka KeroResearch Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, Turku, 20520, Finland.
Joon KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon, 34040, Republic of Korea.
Minho ShongResearch Center for Endocrine and Metabolic Diseases, Division of Endocrinology, Department of Internal Medicine, Chungnam National University School of Medicine, 266 Munhwa-ro, Jung-gu, Daejeon, 35015, Republic of Korea. minhos@cnu.ac.kr.
Chungnam National University · KRCatholic University of Korea · KRSeoul National University Hospital · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KRKorea Advanced Institute of Science and Technology · KRUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsCell Line, TumorCells, CulturedCiliaCRISPR-Cas SystemsHumansMiceMice, Inbred C57BLMutationPhenotypeThyroid NeoplasmsTumor Suppressor ProteinsIFT88 protein, humanTumor Suppressor Proteins

Identifiers

PMID29743590
OpenAlexW2800378317

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.