ReviewBioMed research international2015
PLK-1 Targeted Inhibitors and Their Potential against Tumorigenesis.
Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- PLK1 inhibitors for the treatment of colorectal cancer.Annals of medicine and surgery (2012) · 2025Review
- Small-Molecule Mitotic Inhibitors as Anticancer Agents: Discovery, Classification, Mechanisms of Action, and Clinical Trials.International journal of molecular sciences · 2025Review
- Mitotic kinases are emerging therapeutic targets against metastatic breast cancer.Cell division · 2024Review
- The prognostic values and immune characteristics of polo-like kinases (PLKs) family: A pan-cancer multi-omics analysis.Heliyon · 2024Article
- Review
- Pentafuhalol-B, a Phlorotannin from Brown Algae, Strongly Inhibits the PLK-1 Overexpression in Cancer Cells as Revealed by Computational Analysis.Molecules (Basel, Switzerland) · 2023Article
- Novel Investigational Agents and Pathways That May Influence the Future Management of Acute Myeloid Leukemia.Cancers · 2023Review
- CRISPR-Cas9 knockout screen identifies novel treatment targets in childhood high-grade glioma.Clinical epigenetics · 2023Article
- PELO facilitates PLK1-induced the ubiquitination and degradation of Smad4 and promotes the progression of prostate cancer.Oncogene · 2022Article
- Recent advances in aptamer applications for analytical biochemistry.Analytical biochemistry · 2022Article
- Inhibition of Polo-like Kinase 1 by HMN-214 Blocks Cell Cycle Progression and Inhibits Neuroblastoma Growth.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Differential Expression of Potential Biomarkers of Oral Squamous Cell Carcinoma Development.Head and neck pathology · 2021Article
- Adjunctive Volasertib in Patients With Acute Myeloid Leukemia not Eligible for Standard Induction Therapy: A Randomized, Phase 3 Trial.HemaSphere · 2021Article
- Cytokinesis regulators as potential diagnostic and therapeutic biomarkers for human hepatocellular carcinoma.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Review
- Regulation of the SIAH2-HIF-1 Axis by Protein Kinases and Its Implication in Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- The intensification of anticancer activity of LFM-A13 by erythropoietin as a possible option for inhibition of breast cancer.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Article
- Up-and-Coming Experimental Drug Options for Metastatic Colorectal Cancer.Journal of experimental pharmacology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitotic kinases are the key components of the cell cycle machinery and play vital roles in cell cycle progression. PLK-1 (Polo-like kinase-1) is a crucial mitotic protein kinase that plays an essential role in both the onset of G2/M transition and cytokinesis. The overexpression of PLK-1 is strongly correlated with a wide spectrum of human cancers and poor prognosis. The (si)RNA-mediated depletion of PLK-1 arrests tumor growth and triggers apoptosis in cancer cells without affecting normal cells. Therefore, PLK-1 has been selected as an attractive anticancer therapeutic drug target. Some small molecules have been discovered to target the catalytic and noncatalytic domains of PLK-1. These domains regulate the catalytic activation and subcellular localization of PLK-1. However, while PLK-1 inhibitors block tumor growth, they have been shown to cause severe adverse complications, such as toxicity, neutropenia, and bone marrow suppression during clinical trials, due to a lack of selectivity and specificity within the human kinome. To minimize these toxicities, inhibitors should be tested against all protein kinases in vivo and in vitro to enhance selectivity and specificity against targets. Here, we discuss the potency and selectivity of PLK-1-targeted inhibitors and their molecular interactions with PLK-1 domains.
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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.