ArticleOncogene2020
Suppression of the solar ultraviolet-induced skin carcinogenesis by TOPK inhibitor HI-TOPK-032.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Evidence for PDZ-Binding Kinase in Lung Disease With an Emphasis on PAH.Pulmonary circulation · 2026Review
- Deletion of p53-Related Protein Kinase Suppresses Solar UV-Induced Photocarcinogenesis by Inhibiting PD-L1 Expression and Enhancing CD8 T-Cell Infiltration.The Journal of investigative dermatology · 2026Article
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Article
- Sinomenine Inhibits TOPK To Ameliorate Psoriasiform Dermatitis.ACS omega · 2025Article
- Ultraviolet (UV) radiation: a double-edged sword in cancer development and therapy.Molecular biomedicine · 2024Review
- The Therapeutic Role of Genistein in Perimenopausal and Postmenopausal Women.The Journal of clinical and aesthetic dermatology · 2024Review
- Phosphorylation of PBK at Thr9 by CDK5 correlates with invasion of prolactinomas.CNS neuroscience & therapeutics · 2024Article
- Comprehensive Physicochemical Characterization, In Vitro Membrane Permeation, and In Vitro Human Skin Cell Culture of a Novel TOPK Inhibitor, HI-TOPK-032.International journal of molecular sciences · 2023Article
- TOPK promotes the growth of esophageal cancer in vitro and in vivo by enhancing YB1/eEF1A1 signal pathway.Cell death & disease · 2023Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- T-LAK cell-originated protein kinase (TOPK): an emerging prognostic biomarker and therapeutic target in osteosarcoma.Molecular oncology · 2021Article
- Functional genomics for breast cancer drug target discovery.Journal of human genetics · 2021Review
- Review
- PBK phosphorylates MSL1 to elicit epigenetic modulation of CD276 in nasopharyngeal carcinoma.Oncogenesis · 2021Article
- PDZ Binding Kinase/T-LAK Cell-Derived Protein Kinase Plays an Oncogenic Role and Promotes Immune Escape in Human Tumors.Journal of oncology · 2021Article
- T-LAK cell-originated protein kinase (TOPK) is a Novel Prognostic and Therapeutic Target in Chordoma.Cell proliferation · 2020Article
- Are FDA-Approved Sunscreen Components Effective in Preventing Solar UV-Induced Skin Cancer?Cells · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Nonmelanoma skin cancer (NMSC) such as cutaneous squamous cell carcinoma (cSCC) is caused by solar ultraviolet (SUV) exposure and is the most common cancer in the United States. T-LAK cell-originated protein kinase (TOPK), a serine-threonine kinase is activated by SUV irradiation and involved in skin carcinogenesis. Strategies with research focusing on the TOPK signaling pathway and targeted therapy in skin carcinogenesis may helpful for the discovery of additional treatments against skin cancer. In this study, we found that TOPK can directly bind to and phosphorylate c-Jun (as one of the core member of AP-1) at Ser63 and Ser73 after SSL exposure in a JNKs-independent manner. TOPK knocking down, or HI-TOPK-032 (TOPK specific inhibitor) attenuated colony formation and cell proliferation of skin cancer cells. Phosphorylated levels of c-Jun were overexpressed in human AK and cSCC compared with normal skin tissues, and HI-TOPK-032 inhibited the phosphorylation of c-Jun in SCC cell line in a dose-dependent manner. Furthermore, HI-TOPK-032 decreased SSL-induced AP-1 transactivation activity. Moreover, acute SSL-induced inflammation was attenuated by the topical application of HI-TOPK-032 in SKH1 hairless mice. Importantly, HI-TOPK-032 suppressed chronic SSL-induced skin carcinogenesis and c-Jun phosphorylation levels in SKH1 hairless mice. Our results demonstrate that TOPK can phosphorylate and activate c-Jun at Ser63 and Ser73 in the process of skin carcinogenesis and HI-TOPK-032 could be used as a potential chemopreventive drug against cSCC development.
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Registered trials
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.