ArticleImmunity, inflammation and disease2023
TBK1 promotes thyroid cancer progress by activating the PI3K/Akt/mTOR signaling pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 18 citations in OpenAlex.
- CXCR6 and its correlated G protein-coupled receptors and PI3K-AKT pathways were associated with the progression of thyroid cancer.BMC cancer · 2026Article
- Periostin promotes papillary thyroid carcinoma progression by modulating mTOR/AKT pathway.Translational cancer research · 2026Article
- Saikosaponin D overcomes gemcitabine resistance in pancreatic cancer via AKT/mTOR pathway inhibition and synergistic induction of apoptosis and autophagy.Oncology reports · 2026Article
- Myc-associated zinc finger protein drives colorectal cancer metastasis through activating ubiquitin like with ring finger protein one.World journal of gastrointestinal oncology · 2025Article
- Molecular Markers for Thyroid Cancer Diagnosis: Insights from MAPK Pathway Gene Expression Analysis.Biomedicines · 2025Article
- BBOX1 restrains TBK1-mTORC1 oncogenic signaling in clear cell renal cell carcinoma.Nature communications · 2025Article
- Investigation of Scutellaria Barbata's immunological mechanism against thyroid cancer using network pharmacology and experimental validation.Scientific reports · 2025Article
- TBK1 inhibitor amlexanox exerts anti-cancer effects against endometrial cancer by regulating AKT/NF-κB signaling.International journal of biological sciences · 2025Article
- HIF1A acts as target of XiHuang Pill in the treatment of papillary thyroid cancer by regulating dedifferentiation.Frontiers in chemistry · 2025Article
- TBK1 mutation and its role in frontotemporal dementia and amyotrophic lateral sclerosis in Brazilian families.Dementia & neuropsychologia · 2025Review
- miR-144-3p Targets GABRB2 to Suppress Thyroid Cancer Progression In Vitro.Cell biochemistry and biophysics · 2024Article
- Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma.Communications biology · 2024Article
- In Silico Insights: QSAR Modeling of TBK1 Kinase Inhibitors for Enhanced Drug Discovery.Journal of chemical information and modeling · 2024Article
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- TBK1 promotes thyroid cancer progress by activating the PI3K/Akt/mTOR signaling pathway.Immunity, inflammation and disease · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThyroid cancer has received increasing attention; however, its detailed pathogenesis and pathological processes remain unclear. We investigated the role of TANK-binding kinase 1 (TBK1) in the progression of thyroid cancer.
methodsThe expression of TBK1 in thyroid cancer and normal control tissues was analyzed using real-time quantitative polymerase chain reaction. The function of TBK1 on thyroid cancer cells was detected using MTT, colony formation, wound healing, and Transwell assays. The xenograft assay was carried out to check on the role of TBK1 in thyroid cancer.
resultsTBK1 was highly expressed in thyroid tumors. High expression of TBK1 raised viability, proliferation, migration, and invasion of thyroid cancer cells. Gene set enrichment analysis revealed that TBK1 activated the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin pathway. In addition, Myc-associated zinc finger protein (MAZ) was overexpressed in thyroid cancer and transcriptionally activated BK1. MAZ silence reversed the effects of TBK1 overexpression on thyroid cancer progression. Cotransfection with MAZ small-interfering RNA(siRNA) and TBK1 siRNA did not strengthen the inhibitory effect of TBK1 silencing on the thyroid cancer cells. The xenograft tumor assay showed that TBK1 short hairpinRNA inhibited tumor growth.
conclusionMAZ silencing inhibited tumor progress of thyroid cancer cells, whereas this inhibitory effect was reversed by TBK1 overexpression.
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