ArticleOncoTargets and therapy2019
PLK1 contributes to autophagy by regulating MYC stabilization in osteosarcoma cells.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Paediatric therapeutic development workshop on osteosarcoma.British journal of cancer · 2026Review
- Reoviruses hijack the SMARCB1-MYC transcriptional regulation complex to activate autophagy for persistent viral infection in leafhopper vector.PLoS pathogens · 2025Article
- A review of synergistic strategies in cancer therapy: resveratrol-loaded hydrogels for targeted and multimodal treatment.Discover oncology · 2025Review
- USP10 promotes the progression and attenuates gemcitabine chemotherapy sensitivity via stabilizing PLK1 in PDAC.Cell death & disease · 2025Article
- Temporal myc dynamics permit mitotic bypass, promoting polyploid phenotypes.Cancer letters · 2025Review
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
- Onvansertib and Navitoclax Combination as a New Therapeutic Option for Mucinous Ovarian Carcinoma.International journal of molecular sciences · 2025Article
- PLK1 in cancer therapy: a comprehensive review of immunomodulatory mechanisms and therapeutic opportunities.Frontiers in immunology · 2025Review
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Trends and future directions of autophagy in osteosarcoma: A bibliometric analysis.Open medicine (Warsaw, Poland) · 2024Review
- Combined Inhibition ofInternational journal of molecular sciences · 2023Article
- Kinome-wide CRISPR-Cas9 knockout screens revealed PLK1 as a therapeutic target for osteosarcoma.Cell death discovery · 2023Article
- When Just One Phosphate Is One Too Many: The Multifaceted Interplay between Myc and Kinases.International journal of molecular sciences · 2023Review
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Targeting autophagy process in center nervous trauma.Frontiers in neuroscience · 2023Review
- Onvansertib inhibits the proliferation and improves the cisplatin-resistance of lung adenocarcinoma via β-catenin/c-Myc signaling pathway.American journal of cancer research · 2023Article
- The mitotic regulator polo-like kinase 1 as a potential therapeutic target for c-Myc-overexpressing canine osteosarcomas.Veterinary and comparative oncology · 2022Article
- Present and Future Perspective on PLK1 Inhibition in Cancer Treatment.Frontiers in oncology · 2022Review
- TP53 in Biology and Treatment of Osteosarcoma.Cancers · 2021Review
- The Contribution of Autophagy and LncRNAs to MYC-Driven Gene Regulatory Networks in Cancers.International journal of molecular sciences · 2021Review
Corrections and comments
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPLK1, a typical PLK protein, is the main driver of cancer cell growth and proliferation. It is an inhibitor of the protein kinases that is currently being investigated in clinical studies. It is often used as a tumor marker, as high PLK1 expression correlates with poor prognosis in cancer. Overexpression of MYC is a hallmark of many human cancers. MYC modulates the transcription of thousands of genes that required to coordinate a series of cellular processes, including those essential for growth, proliferation, differentiation, self-renewal and apoptosis. To date, functions of PLK1 and MYC on tumor are mostly studied in separate researches, and studies on their mutual crosstalk are lacking. PURPOSE: To investigate the mechanism of PLK1 and MYC in regulating progress of osteosarcoma.
methodsProtein level was examined using Western blot. Animal experiments were performed with female FOX CHASE severe combined immunodeficient mice. Mice were randomly divided into experimental or control groups.
resultsPLK1 or MYC promoted the proliferation of osteosarcoma cells through the autophagy pathway. PLK1 contributed to MYC protein stabilization. PLK1 inhibition enhanced MYC degradation in osteosarcoma cells. PLK1 inhibition led to a marked decline in MYC protein abundance. The representative MYC target genes were deregulated by PLK1 inhibitors. BI2536 treatment caused a significant delay in xenograft tumor growth in mice injected with U-2 OS cells subcutaneously, with lower mean tumor weight compared to the control group.
conclusionPLK1 is crucial for MYC stabilization. It promotes cell proliferation by autophagy pathway in osteosarcoma cells. Data validate PLK1 as a potential therapeutic target in osteosarcoma caused by MYC-amplified.
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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.