ArticleOncology letters2018
Plk1 promotes the migration of human lung adenocarcinoma epithelial cells via STAT3 signaling.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Integration of machine learning-based screening approaches and single-cell sequencing technique to identify cancer stemness genes associated with radiotherapy resistance in lung adenocarcinoma.Discover oncology · 2026Article
- The effect of PARP and PLK1 dual inhibition on the expression of important protein signaling pathways, DNA damage, and molecular docking scores against MCF-7 and MDA-MB-231 breast cancer cell lines.Irish journal of medical science · 2026Article
- Targeting PLK1 Reduces MMP10 to Enhance Radiosensitivity in HPV- Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Activated PLK1 promotes the migration and invasion of polyploid giant cancer cells with daughter cells via β-catenin/STAT3 signaling pathway.Human cell · 2025Article
- Exploration of telomere-related biomarkers for lung adenocarcinoma and targeted drug prediction.Discover oncology · 2025Article
- PLK1 phosphorylates RhoGDI1 and promotes cancer cell migration and invasion.Cancer cell international · 2024Article
- Overview of Cancer Metabolism and Signaling Transduction.International journal of molecular sciences · 2022Review
- Development of a nanoparticle-based immunotherapy targeting PD-L1 and PLK1 for lung cancer treatment.Nature communications · 2022Article
- Development and validation of endoplasmic reticulum stress-related eight-gene signature for predicting the overall survival of lung adenocarcinoma.Translational cancer research · 2022Article
- Synergistic apoptotic effect of miR-183-5p and Polo-Like kinase 1 inhibitor NMS-P937 in breast cancer cells.Cell death and differentiation · 2022Article
- A more novel and powerful prognostic gene signature of lung adenocarcinoma determined from the immune cell infiltration landscape.Frontiers in surgery · 2022Article
- Essential function and targets of BMP signaling during midbrain neural crest delamination.Developmental biology · 2021Article
- Genomics and Prognosis Analysis of NFrontiers in genetics · 2021Article
- Identifying the Effect of Ursolic Acid Against Triple-Negative Breast Cancer: Coupling Network Pharmacology With Experiments Verification.Frontiers in pharmacology · 2021Article
- Analyses of expressions and prognostic values of Polo-like kinases in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2020Article
- PLK1 and EGFR targeted nanoparticle as a radiation sensitizer for non-small cell lung cancer.Cancer letters · 2019Article
- Polo-like kinase 1 inhibition in NSCLC: mechanism of action and emerging predictive biomarkers.Lung Cancer (Auckland, N.Z.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinase (Plk)1 contributes to the development of human cancer via multiple mechanisms, such as promoting the migration of cancer cells. However, the mechanistic basis for the regulation of cell migration by Plk1 remains unknown. To address this question, the present study investigated the effect of Plk1 inhibition on the migration of human lung adenocarcinoma epithelial A549 cells and the molecular factors involved. A549 cells were treated with the Plk1 inhibitor, BI2536, and cell migration was evaluated with the wound-healing assay. The expression of matrix metallopeptidase (MMP)2, vascular endothelial growth factor (VEGF)A, total and phosphorylated signal transducer and activator of transcription (STAT)3 was assessed by western blotting and reverse transcription-polymerase chain reaction following Plk1 knockdown and/or STAT3 overexpression. The interaction between Plk1 and STAT3 was evaluated by co-immunoprecipitation. The levels of MMP2 and VEGFA were decreased by treatment with Plk1 inhibitor. The phosphorylation of STAT3, which acts upstream of MMP2 and VEGFA, was also decreased by Plk1 knockdown, an effect that was abrogated by STAT3 overexpression. In addition, Plk1 was detected to bind with STAT3 either directly or as part of a complex by co-immunoprecipitation experiments. These results indicated that Plk1 may promote the migration of A549 cells via regulation of STAT3 signaling.
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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.