ArticleOncotarget2016
Phosphorylation of TOPK at Y74, Y272 by Src increases the stability of TOPK and promotes tumorigenesis of colon.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Advances in T-Lymphokine-activated Killer Cell-originated Protein Kinase Research in Cancer Over the Past Thirty Years.Journal of cancer prevention · 2026Review
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Integrating Inflammatory and Epigenetic Signatures in IBD-Associated Colorectal Carcinogenesis: Models, Mechanisms, and Clinical Implications.International journal of molecular sciences · 2025Review
- The SRC-TOPK positive feedback loop promotes RB1 phosphorylation and drives the development of lung squamous cell carcinoma.Acta biochimica et biophysica Sinica · 2025Article
- Correlation study of PBK/TOPK expression, prognosis, and immune infiltration in breast cancer.Scientific reports · 2025Article
- Sinomenine Inhibits TOPK To Ameliorate Psoriasiform Dermatitis.ACS omega · 2025Article
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- MMP-9-dependent proteolysis of the histone H3 N-terminal tail: a critical epigenetic step in driving oncogenic transcription and colon tumorigenesis.Molecular oncology · 2024Article
- FYN/TOPK/HSPB1 axis facilitates the proliferation and metastasis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Inhibiting ALK-TOPK signaling pathway promotes cell apoptosis of ALK-positive NSCLC.Cell death & disease · 2022Article
- TOPK/PBK is phosphorylated by ERK2 at serine 32, promotes tumorigenesis and is involved in sorafenib resistance in RCC.Cell death & disease · 2022Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- VprBP directs epigenetic gene silencing through histone H2A phosphorylation in colon cancer.Molecular oncology · 2021Article
- Review
- Review
- Histone Modifications and their Role in Colorectal Cancer (Review).Pathology oncology research : POR · 2020Review
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- Acetylshikonin suppressed growth of colorectal tumour tissue and cells by inhibiting the intracellular kinase, T-lymphokine-activated killer cell-originated protein kinase.British journal of pharmacology · 2020Article
- Targeting the COX2/MET/TOPK signaling axis induces apoptosis in gefitinib-resistant NSCLC cells.Cell death & disease · 2019Article
- Off-target toxicity is a common mechanism of action of cancer drugs undergoing clinical trials.Science translational medicine · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-LAK cell-originated protein kinase (TOPK), a serine/threonine protein kinase, is highly expressed in a variety of tumors and associated with a poor prognosis of human malignancies. However, the activation mechanism of TOPK is still unrevealed. Herein, first we found that Src directly bound with and phosphorylated TOPK at Y74 and Y272 in vitro. Anti-phospho-TOPK at Y74 was prepared, the endogenous phosphorylation of TOPK at Y74 was detected in colon cancer cells, and the phosphorylation was inhibited in cells expressing low levels of Src. Subsequently, we stably transfected Y74 and Y272 double mutated TOPK (TOPK-FF) into JB6 or SW480 cells, and observed that both the anchorage-independent growth ability and tumorigenesis of TOPK-FF cells were suppressed compared with those of wild type TOPK (TOPK-WT) ex vivo and in vivo. The phosphorylation level of TOPK substrate, Histone H3 at Ser10 also decreased dramatically ex vivo or in vivo. Moreover, we showed that Src could inhibit the ubiquitination of TOPK. Transiently expressed TOPK-WT was more stable than TOPK-FF in pause and chase experiment. Endogenous TOPK was more stable in Src wild type (Src+/+) MEFs than in Src knockout (Src-/-). Taken together, our results indicate that Src is a novel upstream kinase of TOPK. The phosphorylation of TOPK at Y74 and Y272 by Src increases the stability and activity of TOPK, and promotes the tumorigenesis of colon cancer. It may provide opportunities for TOPK based prognosis and targeted therapy for colon cancer patients.
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