ArticleOncotarget2015
PLK1 is a critical determinant of tumor cell sensitivity to CPT11 and its inhibition enhances the drug antitumor efficacy in squamous cell carcinoma models sensitive and resistant to camptothecins.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- 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
- Manipulation of cancer cell pyroptosis for therapeutic approaches: challenges and opportunities.Biomarker research · 2025Review
- Effectiveness of irinotecan plus trabectedin on a desmoplastic small round cell tumor patient-derived xenograft.Disease models & mechanisms · 2023Article
- PLK1 inhibition-based combination therapies for cancer management.Translational oncology · 2022Review
- Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination.Molecular cell · 2021Article
- Polo like kinase 1 expression in cervical cancer tissues generated from multiple detection methods.PeerJ · 2020Article
- Volasertib preclinical activity in high-risk hepatoblastoma.Oncotarget · 2019Article
- Dimeric Prodrug Self-Delivery Nanoparticles with Enhanced Drug Loading and Bioreduction Responsiveness for Targeted Cancer Therapy.ACS applied materials & interfaces · 2018Article
- A lethal synergy induced by phellinus linteus and camptothecin11 in colon cancer cells.Oncotarget · 2018Article
- Nanocrystals of a new camptothecin derivative WCN-21 enhance its solubility and efficacy.Oncotarget · 2017Article
- Dasatinib synergises with irinotecan to suppress hepatocellular carcinoma via inhibiting the protein synthesis of PLK1.British journal of cancer · 2017Article
- Article
- Polo-like kinases and UV-induced skin carcinogenesis: What we know and what's next.Photochemistry and photobiologyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrinsic and acquired tumor drug resistance limits the therapeutic efficacy of camptothecins (CPTs). Downregulation of the mitotic kinase PLK1 was found associated with apoptosis induced by SN38 (CPT11 active metabolite). We investigated the role of PLK1 in the cell response to CPTs in squamous cell carcinoma (SCC) and pediatric sarcoma cell lines and explored the therapeutic potential of the combination of CPT11 and the PLK1 inhibitor BI2536 in CPT-sensitive and -resistant tumor models. Gain- and loss-of-function experiments established a direct role for PLK1 in counteracting SN38 antiproliferative and pro-apoptotic effects. The ability to activate an efficient G2/M cell cycle checkpoint allowing PLK1 ubiquitination and degradation was found associated with SN38-induced apoptosis in SCC cells. However, the synergistic interaction between SN38 and BI2536 enhanced apoptosis in cell lines both sensitive and resistant to SN38-induced apoptotic cell death. A well-tolerated CPT11/BI2536 cotreatment resulted in improved antitumor effect against SCC xenografts in mice compared to single agent treatments. The increased apoptosis induction was reflected in a high rate of complete responses and cures in mice harboring SCC, including tumors with intrinsic or acquired resistance to CPTs. PLK1 inhibition represents a promising strategy to improve the antitumor efficacy of CPT11-based regimens.
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