ArticleChinese journal of cancer2016
Attenuated LKB1-SIK1 signaling promotes epithelial-mesenchymal transition and radioresistance of non-small cell lung cancer cells.
Article in Chinese journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 84 citations in OpenAlex.
- Single-Cell Sequencing Reveals the Role of Radiation-Induced Stemness-Responsive Cancer Cells in the Development of Radioresistance.International journal of molecular sciences · 2025Article
- LKB1 Mutations Enhance Radiosensitivity in Non-Small Cell Lung Cancer Cells by Inducing G2/M Cell Cycle Phase Arrest.Current molecular medicine · 2025Article
- Role of SIK1 in tumors: Emerging players and therapeutic potentials (Review).Oncology reports · 2024Review
- Article
- Roles of salt‑inducible kinases in cancer (Review).International journal of oncology · 2023Review
- Down-regulation and Clinic-pathological Correlation of SIK-1 and SIK-1-LNC in Non-small Cell Lung Cancer PatientsAsian Pacific journal of cancer prevention : APJCP · 2023Article
- SIK1 suppresses colorectal cancer metastasis and chemoresistance via the TGF-β signaling pathway.Journal of Cancer · 2023Article
- Review: Mechanisms and perspective treatment of radioresistance in non-small cell lung cancer.Frontiers in immunology · 2023Review
- Roles of NExperimental hematology & oncology · 2022Review
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Role ofOncology letters · 2022Review
- BMI1 promotes osteosarcoma proliferation and metastasis by repressing the transcription of SIK1.Cancer cell international · 2022Article
- GATA3 Exerts Distinct Transcriptional Functions to Regulate Radiation Resistance in A549 and H1299 Cells.Oxidative medicine and cellular longevity · 2022Article
- LKB1 inhibits proliferation, metastasis and angiogenesis of thyroid cancer by upregulating SIK1.Journal of Cancer · 2022Article
- Review
- Role of SIK1 in the transition of acute kidney injury into chronic kidney disease.Journal of translational medicine · 2021Article
- SIKs suppress tumor function and regulate drug resistance in breast cancer.American journal of cancer research · 2021Article
- Identification of Key Genes Mutations Associated With the Radiosensitivity by Whole Exome Sequencing in Pancreatic Cancer.Frontiers in oncology · 2021Article
- Article
- The potent roles of salt-inducible kinases (SIKs) in metabolic homeostasis and tumorigenesis.Signal transduction and targeted therapy · 2020Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRadiotherapy is one of the main therapeutic approaches for non-small cell lung cancer (NSCLC). However, radioresistant cancer cells can eventually cause tumor relapse and even fatal metastasis. It is thought that radioresistance and metastasis could be potentially linked by epithelial-mesenchymal transition (EMT). In this study, we established radioresistant NSCLC cells to investigate the potential relationship among radioresistance, EMT, and enhanced metastatic potential and the underlying mechanism involving liver kinase B1 (LKB1)-Salt-inducible kinase 1 (SIK1) signaling.
methodsThe radioresistant cell lines A549R and H1299R were generated by dose-gradient irradiation of the parental A549 and H1299 cells. The radioresistance/sensitivity was evaluated by Cell Counting Kit-8 assay, apoptosis analysis, and/or clonogenic cell survival assay. The EMT phenotype and the signaling change were assessed by Western blotting. The abilities of invasion and migration were evaluated by transwell assays and wound healing assays.
resultsThe radioresistant cell lines A549R and H1299R displayed mesenchymal features with enhanced invasion and migration. Mechanistically, A549R and H1299R cells had attenuated LKB1-SIK1 signaling, which leaded to the up-regulation of Zinc-finger E-box-binding homeobox factor 1 (ZEB1)--a transcription factor that drives EMT. Re-expression of LKB1 in A549R cells reversed the EMT phenotype, whereas knockdown of LKB1 in H1299R cells further promoted the EMT phenotype. Moreover, re-expression of LKB1 in A549 cells increased the radiosensitivity, whereas knockdown of LKB1 in H1299 cells decreased the radiosensitivity.
conclusionsOur findings suggest that attenuated LKB1-SIK1 signaling promotes EMT and radioresistance of NSCLC cells, which subsequently contributes to the enhanced metastatic potential. Targeting the LKB1-SIK1-ZEB1 pathway to suppress EMT might provide therapeutic benefits.
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