ArticleBioengineered2022
Knockdown of KRAB domain-associated protein 1 suppresses the proliferation, migration and invasion of thyroid cancer cells by regulating P68/DEAD box protein 5.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- Global epidemiology of thyroid cancer: trends in incidence, mortality, and DALYs from 1990 to 2021.Open medicine (Warsaw, Poland) · 2026Article
- Multifaceted role ofMedComm · 2024Review
- Review
- Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33.Human cell · 2023Article
- The role of tripartite motif-containing 28 in cancer progression and its therapeutic potentials.Frontiers in oncology · 2023Review
- Pan-cancer analysis of the prognostic and immunological roles ofFrontiers in genetics · 2022Article
Corrections and comments
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KRAB domain-associated protein 1 (KAP-1) has been reported to be an oncogene in diverse tumors. KAP-1 was found to have abundant existence in malignant thyroid tissues, but its role in thyroid cancer hasn't been elucidated clearly. This study was carried out to explore the role of KAP-1 in thyroid cancer, and to clarify its molecular mechanism. The expressions of KAP-1 and P68/DEAD box protein 5 (DDX5) were assessed under the help of qRT-PCR and western blot. Then, we downregulated KAP-1 or upregulated DDX5 by cell transfection in TPC-1 cells. A series of cellular experiments on proliferation, apoptosis, migration and invasion were conducted with CCK-8, EdU, TUNEL, wound-healing and Transwell assays. Besides, the relationship between KAP-1 and DDX5 was verified by co-immunoprecipitation (Co-IP). The results showed that both of KAP-1 and DDX5 were upregulated in thyroid cancer cells. Loss-of-function experiments revealed that KAP-1 knockdown imparted suppressive effects on cell proliferation, migration and invasion, but promoted cell apoptosis. Additionally, KAP-1 was demonstrated to interact with DDX5 and positively regulate DDX5 expression. The following rescued experiments exhibited that the inhibitory effects of KAP-1 knockdown on cellular activities of thyroid cancer and Wnt/β-catenin signaling were also partly reversed by DDX5 overexpression. Moreover, activation of Wnt/β-catenin signaling retarded the anti-tumor activity of KAP-1 knockdown. In conclusion, the data in this study disclosed that KAP-1 silence helped to repress the cell proliferation, migration and invasion by degrading DDK5, so as to hinder the development of thyroid cancer.
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