ArticleCell death & disease2019
STYK1 promotes tumor growth and metastasis by reducing SPINT2/HAI-2 expression in non-small cell lung cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- AJournal of gastrointestinal oncology · 2026Article
- Membrane-Anchored Serine Protease Inhibitors: Physiological Functions, Mechanisms, and Roles in Cancer.International journal of molecular sciences · 2026Review
- STYK1 as a targetable vulnerability enhances the efficacy of anti-PD-L1 therapy in pancreatic cancer.Journal of gastroenterology · 2025Article
- CircSPINT2 confers sensitivity to osimertinib via hsa-miR-1296-3p/RBP1 axis and inhibits NSCLC progression.Molecular therapy. Oncology · 2025Article
- Serine/threonine/tyrosine kinase 1 drives pancreatic carcinogenesis via GSK3β sequestration-mediated Wnt/β-catenin pathway hyperactivation.Signal transduction and targeted therapy · 2025Article
- Refined Procedure to Purify and Sequence Circulating Cell-Free DNA in Prostate Cancer.International journal of molecular sciences · 2025Article
- Combined proteomics and metabolomics analysis reveal the effect of a training course on the immune function of Chinese elite short-track speed skaters.Immunity, inflammation and disease · 2024Article
- Gliomedin drives gastric cancer cell proliferation and migration, correlating with a poor prognosis.Heliyon · 2024Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Bibliometric analysis of ferroptosis: a comprehensive evaluation of its contribution to lung cancer.Frontiers in genetics · 2024Article
- SPINT2 is involved in the proliferation, migration and phenotypic switching of aortic smooth muscle cells: Implications for the pathogenesis of thoracic aortic dissection.Experimental and therapeutic medicine · 2023Article
- Ferroptosis in lung cancer: a novel pathway regulating cell death and a promising target for drug therapy.Cell death discovery · 2023Review
- Nanofat lysate ameliorates pain and cartilage degradation of osteoarthritis through activation of TGF-β-Smad2/3 signaling of chondrocytes.Frontiers in pharmacology · 2023Article
- High-fat intake reshapes the circadian transcriptome profile and metabolism in murine meibomian glands.Frontiers in nutrition · 2023Article
- Characterizing the secretome of EGFR mutant lung adenocarcinoma.Frontiers in oncology · 2023Article
- STYK1/NOK affects cell cycle late mitosis and directly interacts with anaphase-promoting complex activator CDH1.Heliyon · 2022Article
- Melatonin inhibits ESCC tumor growth by mitigating the HDAC7/β-catenin/c-Myc positive feedback loop and suppressing the USP10-maintained HDAC7 protein stability.Military Medical Research · 2022Article
- The EGFR-STYK1-FGF1 axis sustains functional drug tolerance to EGFR inhibitors in EGFR-mutant non-small cell lung cancer.Cell death & disease · 2022Article
- Mesenchymal-to-epithelial transition of osteoblasts induced by Fam20c knockout.Genes & genomics · 2022Article
- Down regulated oncogeneAnnals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. However, the molecular mechanisms underlying NSCLC progression remains not fully understood. In this study, 347 patients with complete clinicopathologic characteristics who underwent NSCLC surgery were recruited for the investigation. We verified that elevated serine threonine tyrosine kinase 1 (STYK1) or decreased serine peptidase inhibitor Kunitz type 2 (SPINT2/HAI-2) expression significantly correlated with poor prognosis, tumor invasion, and metastasis of NSCLC patients. STYK1 overexpression promoted NSCLC cells proliferation, migration, and invasion. STYK1 also induced epithelial-mesenchymal transition by E-cadherin downregulation and Snail upregulation. Moreover, RNA-seq, quantitative polymerase chain reaction (qRT-PCR), and western blot analyses confirmed that STYK1 overexpression significantly decreased the SPINT2 level in NSCLC cells, and SPINT2 overexpression obviously reversed STYK1-mediated NSCLC progression both in vitro and in vivo. Further survival analyses showed that NSCLC patients with high STYK1 level and low SPINT2 level had the worst prognosis and survival. These results indicated that STYK1 facilitated NSCLC progression via reducing SPINT2 expression. Therefore, targeting STYK1 and SPINT2 may be a novel therapeutic strategy for NSCLC.
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