ArticleFEBS open bio2020
LMTK3 promotes tumorigenesis in bladder cancer via the ERK/MAPK pathway.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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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
23 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- LMTK3 as a spatially regulated and stage-dependent biomarker in epithelial ovarian tumorigenesis.Molecular therapy. Oncology · 2026Article
- The Insulin-Urothelial Axis: Evaluating Insulin Resistance as a Convergent Driver of Bladder Cancer Across Diverse Risk Factor Profiles.International journal of molecular sciences · 2026Review
- Post-translational modifications: Principal regulators of bladder cancer.Molecular biology reports · 2026Review
- Using transcriptomics and molecular docking to uncover the pharmacological targets and its associated biological mechanisms of paeoniflorigenone in treating bladder cancer.Discover oncology · 2026Article
- Orosomucoid 1 interacts with S100A12 and activates ERK signalling to expedite the advancement of bladder cancer.Cell adhesion & migration · 2025Article
- Research progress on the role of AGC kinase family in bladder cancer.Discover oncology · 2025Review
- m7G-related gene signatures determine prognosis in triple-negative breast cancer.Scientific reports · 2025Article
- Evaluation of the Association between LMTK3 Gene Polymorphism and Breast Cancer Risk in the Indian Population.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Inotodiol induces hepatocellular carcinoma apoptosis by activation of MAPK/ERK pathway.PloS one · 2025Article
- Article
- The lemur tail kinase family in neuronal function and disfunction in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Lemur tail kinase 3 serves as a predictor of patient outcomes and a target for the treatment of ovarian cancer.Molecular therapy. Oncology · 2024Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- MiR-205-3p suppresses bladder cancer progression via GLO1 mediated P38/ERK activation.BMC cancer · 2023Article
- The Inhibitory Properties of a Novel, Selective LMTK3 Kinase Inhibitor.International journal of molecular sciences · 2023Article
- HAPLN3 inhibits apoptosis and promotes EMT of clear cell renal cell carcinoma via ERK and Bcl-2 signal pathways.Journal of cancer research and clinical oncology · 2023Article
- NCAPH promotes cell proliferation and inhibits cell apoptosis of bladder cancer cells through MEK/ERK signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- The multifaceted role of lemur tyrosine kinase 3 in health and disease.Open biology · 2021Review
- Lemur Tyrosine Kinases and Prostate Cancer: A Literature Review.International journal of molecular sciences · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lemur tyrosine kinase 3 (LMTK3) is a key member of the serine-threonine tyrosine kinase family. It plays an important role in breast cancer tumorigenesis and progression. However, its biological role in bladder cancer remains elusive. In this study, we demonstrated that LMTK3 was overexpressed in bladder cancer and was positively correlated with bladder cancer malignancy. High LMTK3 expression predicted poor overall survival. Knockdown of LMTK3 in bladder cancer cells triggered cell-cycle arrest at G2/M phase, suppressed cell growth, and induced cell apoptosis in bladder cancer cells. Furthermore, Transwell assays revealed that reduction of LMTK3 decreased cell migration by regulating the epithelial-to-mesenchymal transition pathway. Conversely, LKTM3 overexpression was shown to promote proliferation and migration of bladder cancer cells. We assessed phosphorylation of MEK and ERK1/2 in bladder cancer cells depleted of LMTK3 and demonstrated a reduced phosphorylation status compared with the control group. Using an MAPK signaling-specific inhibitor, U0126, we could rescue the promotion of proliferation and viability in LMTK3-overexpressing cells. In conclusion, we extend the status of LMTK3 as an oncogene in bladder cancer and provide evidence for its function via the activation of the ERK/MAPK pathway. Thus, targeting LMTK3 may hold potential as a diagnostic and prognostic biomarker and as a possible future treatment for bladder cancer.
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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.